Nan Fang Yi Ke Da Xue Xue Bao = Journal Of Southern Medical University[JOURNAL]
Sun
200 papers
[Transcriptomic characteristics of cervical endplate cartilage in cervical spondylosis and effects of acupotomy on the FGF18/Akt axis with cervical spondylosis].
Liu F, Khaliunaa T, Cao Q … +7 more , Yang Y, Ren C, Zhu J, Zhao X, Cao L, Deng B, Wang X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540691 · Full text
OBJECTIVES: To explore the transcriptomic characteristics of the endplate cartilage of the cervical intervertebral disc in cervical spondylosis (CS) and the effects of acupotomy on expressions of fibroblast growth factor...
OBJECTIVES: To explore the transcriptomic characteristics of the endplate cartilage of the cervical intervertebral disc in cervical spondylosis (CS) and the effects of acupotomy on expressions of fibroblast growth factor 18 (FGF18)/protein kinase B (Akt) axis key molecules. METHODS: Transcriptomic analyses were performed using bioinformatics methods based on the GEO database. In the animal experiment, 24 New Zealand rabbits were randomized equally into control, CS model, and acupotomy groups. In the latter two groups, CS models were established followed 7 days later by acupotomy intervention (once a week for 3 weeks) or no particular treatment. Histopathological changes and cell apoptosis in the intervertebral discs were examined with HE staining and TUNEL assay, and the mRNA expressions of FGF18, FGFR3, and Akt in the intervertebral discs were detected using RT-qPCR; the localization and expressions of FGF18, p-Akt, and Akt proteins were examined with immunohistochemistry. RESULTS: The endplate cartilage in CS exhibited numerous differentially expressed genes enriched in the PI3K-Akt signaling, calcium signaling, and Rap1 signaling pathways. CS rabbits showed obvious changes in the cervical spine curvature and joint degenerations, changes in cervical intervertebral disc texture, thinning of the annulus fibrosus, shrinkage or even absence of the nucleus pulposus, and increased apoptotic cells in the endplate cartilage, which were all obviously alleviated after acupotomy. No significant differences were found in the mRNA expressions of FGF18, FGFR3, and Akt in the cervical intervertebral discs among the 3 groups. Acupotomy significantly increased FGF18 and p-Akt protein expressions and reduced the Akt/p-Akt ratio in the cervical endplate cartilage of CS rabbits. CONCLUSIONS: The cervical endplate cartilage of CS show numerous differentially expressed genes. Acupotomy may delay degenerative changes of the intervertebral discs and improves CS by activating the FGF18/Akt axis to reduce apoptosis of endplate cartilage cells.
[ Mixture alleviates diabetic cardiomyopathy in rats by Sirt3-mediated upregulation of myocardial mitochondrial mitophagy pathway].
Lin X, He Y, Shi H … +2 more , Liu J, Hu H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540690 · Full text
OBJECTIVES: To explore the mechanism of Mixture (SHM) for improving diabetic cardiomyopathy. METHODS: Thirty male SD rats were randomized into 3 groups (=10) for type 2 diabetes mellitus modeling by high-fat and -sugar...
OBJECTIVES: To explore the mechanism of Mixture (SHM) for improving diabetic cardiomyopathy. METHODS: Thirty male SD rats were randomized into 3 groups (=10) for type 2 diabetes mellitus modeling by high-fat and -sugar feeding for 12 weeks and intraperitoneal streptozotocin injection, followed by treatment with daily gavage of normal saline (model group), metformin solution, or SHM extract for 4 weeks, with 10 normally fed rats as the normal control group. Fasting blood glucose and cardiac weight index of the rats were monitored, and their TG, TC, LDL-C, HDL-C, and LDH levels were determined; serum and myocardial levels of BNP, CRP, TNF‑α and IL-6 were detected with ELISA. Myocardial pathological changes and ultrastructures of myocardial mitochondria and autophagosomes were examined with HE and Masson staining and transmission electron microscopy. Myocardial expressions of Sirt3, FoxO3a, PINK1, Parkin, P62, and LC3 mRNAs and proteins were detected with RT-qPCR, Western blotting, and immunohistochemistry. RESULTS: Compared with those in the control group, the rats in the other 3 groups showed significantly increased fasting blood glucose, cardiac weight index, serum TC, TG, LDL-C, LDH, CRP and BNP levels and myocardial levels of TNF‑α and IL-6 with lowered HDL-C level, obvious myocardial and mitochondrial pathologies, and dysregulated expression of Sirt3, FoxO3a, p-FoxO3a, PINK1, Parkin, LC3 and P62. Treatment of the rat models with SHM extract significantly reduced fasting blood glucose level and cardiac weight index, lowered the levels of LDH, CRP, BNP, TNF‑α, IL-6, TC, TG, and LDL-C, increased HDL-C level, alleviated myocardial and mitochondrial damages, promoted autophagosome formation, and improved dysregulation of mitochondrial autophagy-related gene expression, showing similar effects to metformin. CONCLUSIONS: SHM alleviates myocardial damage and improves mitochondrial function in rats with diabetic cardiomyopathy by regulating the mitochondrial autophagy pathway through Sirt3.
[ polysaccharide alleviates cyclophosphamide-induced intestinal barrier dysfunction and inflammation in mice by modulating gut flora].
Zhang Y, Duan Y, Zhang C … +8 more , Yu L, Liu Y, Xing L, Wang L, Yu N, Peng D, Chen W, Wang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540689 · Full text
OBJECTIVES: To investigate the protective effects of polysaccharide (PCP) against cyclophosphamide (CTX)-induced intestinal mucosal injury and its impact on gut flora and their metabolites in mice. METHODS: Adult BALB/C...
OBJECTIVES: To investigate the protective effects of polysaccharide (PCP) against cyclophosphamide (CTX)-induced intestinal mucosal injury and its impact on gut flora and their metabolites in mice. METHODS: Adult BALB/C mice were randomized into normal control group, CTX model group, glutamine (positive control) group, and low-, medium- and high-dose PCP treatment groups. In all but the normal control group, the mice were subjected to modeling of CTX-induced intestinal mucosal injury by intraperitoneal CTX injections for 3 days, followed by treatment with gavage of normal saline, glutamine (300 mg/kg), or PCP at 75, 150, or 300 mg/kg for 7 consecutive days. The colonic expressions of tight junction proteins (occludin and ZO-1), serum endotoxin, D-lactate, and DAO levels, intestinal permeability, colon injury, and colonic cytokine levels (IL-4, IL-22, IL-17A, and IFN-γ mRNA) were assessed. Gut microbiota, short-chain fatty acids (SCFAs; mainly acetates and propionates) and colonic GPR41 expression were analyzed using 16S rRNA sequencing, GC-MS, and Western blotting, respectively. Fecal microbiota transplantation (FMT) experiment was conducted to validate the role of gut microbes in PCP-mediated repair of intestinal injuries. RESULTS: Compared with those in the model group, the mice treated with PCP showed significantly increased colonic occludin and ZO-1 expressions, reduced serum endotoxin, D-lactate and DAO levels, and lowered intestinal permeability with increased colonic expressions of IL-4, IL-22, IL-17A, and IFN-γ mRNA. PCP treatment obviously increased the abundance of , decreased and , increased the contents of acetate and propionate in the colon, and upregulated colonic GPR41 expression. The results of FMT experiment confirmed the crucial role of gut microbes in PCP-mediated repair of CTX-induced intestinal injuries in mice. CONCLUSIONS: PCP can protect against CTX-induced intestinal mucosal injury in mice possibly by modulating gut flora and SCFAs metabolism to enhance intestinal defense capacity.
[Temporal changes of chronic postsurgical pain in mice: the regulatory role of CX3CL1 in the dorsal root ganglion].
Zhao B, Lü Z, Ji D … +6 more , Tian S, Wu Y, Li X, Zhou J, Fang J, Liang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540688 · Full text
OBJECTIVES: To observe temporal changes of pain-related behaviors in mice with chronic postsurgical pain (CPSP) and identify its key mediators in the dorsal root ganglion (DRG). METHODS: In mouse models of CPSP induced b...
OBJECTIVES: To observe temporal changes of pain-related behaviors in mice with chronic postsurgical pain (CPSP) and identify its key mediators in the dorsal root ganglion (DRG). METHODS: In mouse models of CPSP induced by plantar incision (INC) followed by a dorsal foot injection of prostaglandin E2 (PGE2) and sham-operated mice, mechanical paw withdrawal thresholds (PWTs), thermal paw withdrawal latencies (PWLs), and cold withdrawal durations (WDs) were measured at different time points after modeling. Gene expression profiling of the DRG with RNA sequencing was performed on day 1 and day 8 after PGE2 injection. Bioinformatics analyses were conducted to explore the key mediators in the DRG for regulating CPSP, and the candidate genes and proteins were validated using RT-qPCR and ELISA. The effects of intrathecal injection of a CX3CL1-neuralizing antibody or JMS-17-2 (a CX3CR1 antagonist) on CPSP were observed. RESULTS: In CPSP mouse models, incision-induced pain was resolved within 14 days, and PWTs and WDs decreased progressively till day 10 and day 12 after PGE2 injection, respectively, without significant changes in PWLs. RNA-Seq identified 975 differentially expressed genes (DEGs) on day 1 and 895 on day 8 following CPSP modeling, including 524 intersecting DEGs enriched in cell membrane, plasma membrane, and CX3C chemokine receptor binding. Cx3cl1 and Cxcl14 were the top two upregulated chemokine-related DEGs in early CPSP, whose mRNA and protein expression increased significantly in the ipsilateral DRG on day 1 but declined on day 8. Intrathecal injection of the CX3CL1-neutralizing antibody before PGE2 injection prevented CPSP development, while JMS-17-2 partially reversed CPSP during the maintenance phase. CONCLUSIONS: This CPSP mouse model shows persistent mechanical and cold allodynia for at least 10 days after PGE2 injection without significant changes in heat hypersensitivity. CX3CL1 and related chemokine signaling in the DRG may contribute to the development of CPSP.
Identification of immune status subtypes and prognostic analysis of septic patients based on Th1/Th2 cytokine assays.
Sha T, Wang W, Xuan J … +5 more , Wu J, Shi N, He J, Hu H, Zhang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540687 · Full text
OBJECTIVES: Sepsis patients exhibit diverse immune states, making it crucial to identify subtypes with distinct inflammatory profiles through Th1/Th2 cytokine data for personalized treatment and improved prognosis. METHO...
OBJECTIVES: Sepsis patients exhibit diverse immune states, making it crucial to identify subtypes with distinct inflammatory profiles through Th1/Th2 cytokine data for personalized treatment and improved prognosis. METHODS: We retrieved data from sepsis patients who underwent Th1/Th2 cytokine testing in Nanfang Hospital, Southern Medical University from June 1, 2020, to February 1, 2022. An unsupervised K-means clustering method classified participants based on Th1/Th2 cytokine levels, with the primary outcome being the 7-day mortality rate post-ICU admission. Cox proportional hazards and Restricted Mean Survival Time (RMST) analyses were utilized to explore survival outcomes. RESULTS: A total of 321 sepsis patients were included. IL-6 (HR 1.69, 95%CI: 1.22, 2.34) and IL-10 (HR 1.81, 95% : 1.37, 2.40) emerged as independent predictors of 7-day mortality. Unsupervised K-means clustering revealed 3 inflammatory/immune subgroups: Cluster 1 (=166, low inflammatory response), Cluster 2 (=99, moderate inflammatory response with immune suppression), and Cluster 3 (=56, strong inflammatory and immune suppression). Compared to Cluster 1, Clusters 2 and 3 had higher 7-day mortality risks (14.4% 23.2%, HR=4.30, 95% : 1.51-12.26; 14.4% 35.7%, HR=7.32, 95% : 2.57-20.79). CONCLUSIONS: Septic patients in a protective immune response state (Cluster 1) exhibit better short-term prognoses, suggesting the importance of understanding inflammatory/immune states for precise treatment and improved outcomes.
[Clinical application and mechanistic studies of psychedelics for treatment of depression: progress and future challenges].
Xia K, Gao T
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Jan · PMID 41540686 · Full text
Depression is a complex and globally prevalent mental disorder, for which conventional antidepressant medications face limitations such as delayed onset and insufficient efficacy. Classic psychedelics, most notably psilo...
Depression is a complex and globally prevalent mental disorder, for which conventional antidepressant medications face limitations such as delayed onset and insufficient efficacy. Classic psychedelics, most notably psilocybin, have recently emerged as promising candidates for treatment of depression and demonstrated rapid, robust, and sustained antidepressant effects in controlled clinical settings. Their unique mechanisms of action and clinical prospects have become a key research focus in psychiatry and neuroscience. This review synthesizes the latest advances in the field over the past 5 years. Results from multiple randomized controlled trials indicate that a single or limited number of sessions of psychedelic-assisted psychotherapy can induce rapid and durable antidepressant effects in patients with treatment-resistant depression. At the mechanistic level, psychedelics rapidly promote the release of neurotrophic factors, enhance neuroplasticity, and facilitate brain network reorganization, thereby creating a critical "neuroplastic window" for psychotherapeutic intervention. However, the specific molecular and circuit-level mechanisms have not been fully understood with ongoing debate primarily over the 5-HT receptor-dependent hypothesis versus the TrkB neurotrophic pathway-dependent hypothesis. Despite the promising outlook, translational applications of these substances faces several key challenges, including psychedelic-related risks, incomplete mechanistic understanding, lack of standardized treatment protocols, and insufficient long-term safety data. Future research should focus on elucidating the underlying neurobiological mechanisms, developing non-hallucinogenic derivatives, establishing standardized treatment frameworks, and identifying precise biomarkers to advance this therapeutic approach toward safer, more standardized, and personalized clinical implementation.
[Evaluation of coronary microvascular dysfunction for assessing prognosis of ST-segment elevation acute myocardial infarction following reperfusion therapy: insights from QFR-AMR].
Gao S, Han Z, Zeng Q … +6 more , Cheng Z, Wang J, Kang P, Wang H, Li M, Hu S
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429630 · Full text
OBJECTIVES: To assess the risk of major adverse cardiovascular and cerebrovascular events (MACCEs) in patients with ST-segment elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI) by...
OBJECTIVES: To assess the risk of major adverse cardiovascular and cerebrovascular events (MACCEs) in patients with ST-segment elevation myocardial infarction (STEMI) following percutaneous coronary intervention (PCI) by evaluating both the large coronary vessels and coronary microcirculation. METHODS: A total of 507 patients with STEMI undergoing successful percutaneous coronary intervention (PCI) were retrospectively enrolled from two centers. The optimal cut-off value (256.5 mmHg·s·m) of angio-based microvascular resistance (AMR) for predicting MACCEs was determined by ROC analysis. Combined with a quantitative flow ratio (QFR) threshold of 0.80, the patients were classified into 4 groups: Group 1 (QFR≥0.8, AMR<256.5; =271), Group 2 (QFR≥0.8, AMR≥256.5; =140), Group 3 (QFR<0.8, AMR<256.5; =77), and Group 4 (QFR<0.8, AMR≥256.5; =19). The primary endpoint was cardiac death or heart failure readmission within 2 years. RESULTS: Patients with elevated AMR (≥256.5 mmHg·s·m) had a significantly increased risk of MACCEs within two years after PCI (P<0.001). Kaplan-Meier analysis showed the lowest survival rate in patients with both QFR<0.8 and AMR≥256.5 mmHg·s·m. Multiple linear regression analysis suggested that diabetes (<0.001), hyperlipidemia (<0.001), smoking (<0.014), systemic inflammation response index (<0.007), and platelet to lymphocyte ratio (<0.001) were independently associated with elevated AMR levels. Restricted cubic spline regression revealed a non-linear relationship between AMR and MACCEs risk (non-linear <0.001), and the hazard ratio for MACCEs increased markedly for an AMR beyond the threshold of 259.45 mmHg·s·m. CONCLUSIONS: The integrated assessment of QFR and AMR allows effective prediction of MACCEs risk in STEMI patients after PCI, and elevated AMR is an independent predictor of significantly increased risk of MACCEs.
[Causal relationship between gut microbiota and T cell subsets in the development of colorectal cancer: a Mendelian randomization analysis].
Yu Z, Gao J, Sun H … +6 more , Feng Q, Na X, Zhang N, Shen K, Wang Y, Wang X
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429629 · Full text
OBJECTIVES: To investigate the causal relationship between gut microbiota, T-cell function, and the risk of colorectal cancer. METHODS: Gut microbiota data from the MiBioGen database and T-cell and colorectal cancer data...
OBJECTIVES: To investigate the causal relationship between gut microbiota, T-cell function, and the risk of colorectal cancer. METHODS: Gut microbiota data from the MiBioGen database and T-cell and colorectal cancer data from publicly available GWAS datasets were obtained for analyzing the causality between gut microbiota, T-cell subsets, and the risk of colorectal cancer with two-sample Mendelian randomization (MR) analyses, using inverse variance weighting as the primary analytical method supplemented with MR-Egger, weighted median, simple mode, and weighted mode methods. Horizontal pleiotropy was assessed using MR-PRESSO and MR-Egger regression. Cochran's Q test was used to evaluate heterogeneity, and sensitivity analysis was performed using the leave-one-out method. RESULTS: In the Forward MR analysis of gut microbiota and T cells, 11 gut microbiota species showed causal relationships. Six of these species exhibited positive correlations with T cells, including (=0.003), UCG011 (=0.033), UCG004 (0.010), group (=0.005), FCS020 group (=0.028), and (=0.033), and the remaining 5 species showed negative correlations with T cells. Forward MR analysis of T cells and colorectal cancer suggested that CD25CD45RACD4 non-regulatory T cells were negatively correlated with colorectal cancer risk (IVW: OR=0.935, 95% : 0.878-0.995; =0.035). The analysis of gut microbiota and colorectal cancer suggested that 11 gut microbiota species were causally associated with colorectal cancer, and 6 of them ( group, =0.039; Selenomonadales, =0.014; , =0.014; , =0.048; Bifidobacteriales, =0.048; and 1, =0.033) showed positive correlations and the remaining 5 showed negative correlations. CONCLUSIONS: spp. and group spp. are causally associated with both T cell activity and colorectal cancer risk, and the former bacteria induce inactivation of CD25CD45RACD4 non-regulatory T cells to promote colorectal cancer progression, whereas the latter bacteria promote CD25CD45RACD4 non-regulatory T cell activity to inhibit colorectal cancer development.
[PSMD11 overexpression promotes epithelial-mesenchymal transition in gastric cancer and affects patient prognosis].
Zhou R, Yang J, Song B … +5 more , Chen X, Wang L, Wang Y, Zuo L, Zhu B
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429628 · Full text
OBJECTIVES: To investigate the expression of the 26S proteasome non-ATPase regulatory subunit 11 (PSMD11) in gastric cancer and its impact on long-term patient prognosis. M Tumor and adjacent tissue samples were collecte...
OBJECTIVES: To investigate the expression of the 26S proteasome non-ATPase regulatory subunit 11 (PSMD11) in gastric cancer and its impact on long-term patient prognosis. M Tumor and adjacent tissue samples were collected from a cohort of 94 gastric cancer patients treated at our hospital from January, 2016 to December, 2019. Immunohistochemistry was used to detect PSMD11 and Ki67 expression levels in the tissues, whose correlations with clinicopathological parameters and postoperative 5-year survival of the patients were analyzed. PSMD11 expression in gastric cancer was also analyzed using data from the GEPIA and UALCAN databases, while the KM-plotter database was used to predict 5-year survival rates. KEGG and GO enrichment analyses were employed to predict the biological functions and mechanisms of PSMD11. In cultured HGC-27 cells, the effects of PSMD11 knockdown and overexpression on cell migration, invasion and expressions of epithelial-mesenchymal transition (EMT) markers and TGF‑β/Smad pathway proteins were evaluated using scratch wound healing assay, Transwell assay, and Western blotting. RESULTS: Bioinformatic analysis showed that PSMD11 expression was significantly elevated in gastric cancer and positively correlated with Ki67 expression (=0.73, <0.05). Survival analysis suggested that high PSMD11 expression was correlated with a poorer prognosis in gastric cancer patients. Univariate and multivariate Cox regression analyses identified PSMD11 as an independent prognostic risk factor in gastric cancer (HR: 2.167, 95% : 1.159-4.051, =0.015). Enrichment analysis suggested involvement of PSMD11 in EMT and TGF‑β signaling. In HGC-27 cells, PSMD11 overexpression significantly enhanced while PSMD11 knockdown suppressed cell migration and invasion. PSMD11 overexpression significantly increased the expression levels of vimentin, N-cadherin, TGF‑β, and p-Smad2/3 and reduced E-cadherin expression, and PSMD11 knockdown produced the opposite changes. CONCLUSIONS: PSMD11 is overexpressed in gastric cancer and adversely affects patient prognosis likely by driving EMT activation of the TGF-β/Smad signaling pathway.
[Human umbilical cord mesenchymal stem cell grafting alleviates inflammatory response in type 1 diabetic mice by suppressing M1 macrophage polarization through Chi3l1].
Liu X, Xu Y, Sheng H … +1 more , Liu H
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429627 · Full text
OBJECTIVES: To explore the role of Chi3l1 in human umbilical cord mesenchymal stem cell (hUC-MSCs) therapy of type 1 diabetes. METHODS: hUC-MSCs with stable Chi3l1 knockdown (sh-Chi3l1-MSCs) were constructed using a lent...
OBJECTIVES: To explore the role of Chi3l1 in human umbilical cord mesenchymal stem cell (hUC-MSCs) therapy of type 1 diabetes. METHODS: hUC-MSCs with stable Chi3l1 knockdown (sh-Chi3l1-MSCs) were constructed using a lentiviral vector and characterized by flow cytometry and adipogenic and osteogenic induction. In adult C57BL/6J mouse models of streptozotocin-induced T1DM, the therapeutic effects of sh-NC-MSCs and sh-Chi3l1-MSCs grafting were evaluated by observing changes in clinical manifestations, blood glucose, body weight and pancreatic tissue pathologies. Insulin content and macrophage infiltration in the islets were detected using immunohistochemistry and immunofluorescence staining. The effects of these two stem cells on induced polarization of co-cultured mouse bone marrow macrophages were assessed using flow cytometry by detecting the mRNA expressions of iNOS, Arg-1, TNF-α, IL-6, IL-10, IL-13, and IL-1β using qPCR. RESULTS: The constructed sh-Chi3l1-MSCs retained the characteristics of MSCs but showed reduced therapeutic efficacy in T1DM mice. Immunofluorescence staining showed that the number of macrophages in the pancreatic tissue of the mice treated with sh-Chi3l1-MSCs was higher than that in MSCs treatment group. In the co-culture experiments, sh-Chi3l1-MSCs exhibited a lowered capacity to suppress M1 polarization of the macrophages and a reduced efficacy to promote differentiation of M2-type macrophage subset. Analysis with qPCR showed that the expressions of M1 macrophage marker iNOS and the inflammatory factors TNF-α, IL-6, and IL-1β increased, while the expressions of M2 macrophage marker Arg-1 and the cytokines IL-13 and IL-10 were decreased significantly in sh-Chi3l1-MSCs group. CONCLUSIONS: In T1DM mouse models, hUC-MSCs mitigate inflammatory responses by suppressing the production of pro-inflammatory M1-type macrophages Chi3l1.
[Polyphyllin VII inhibits osteosarcoma xenograft growth in mice by inducing ferroptosis upregulating SOHLH1].
Xiao D, Tang H, Yang M … +8 more , Teng H, Liang J, Xie T, Feng W, Liu S, Dai W, Li H, Liu Y
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429626 · Full text
OBJECTIVES: To investigate the inhibitory effect of polyphyllin VII (PP7) on osteosarcoma xenograft growth in mice and explore the underlying molecular mechanism. METHODS: Ultra‑performance liquid chromatography‑tandem m...
OBJECTIVES: To investigate the inhibitory effect of polyphyllin VII (PP7) on osteosarcoma xenograft growth in mice and explore the underlying molecular mechanism. METHODS: Ultra‑performance liquid chromatography‑tandem mass spectrometry was used to analyze the main active components of Paris polyphylla. Six nude mice bearing patient‑derived xenograft (PDX) were randomized into two groups for treatment with 2 mg/kg PP7 gavage or saline every other day for 28 days, and the changes in tumor volume and mass were measured. In cultured 143B and HOS cells, the effect of PP7 treatment (0, 1.25, 2.5, 5, and 10 μmol/L) on cell proliferation was assessed with CCK‑8 assay, and Transwell assays were employed to examine the changes in cell migration and invasion. The target of PP7 was predicted by integrated analyses with single‑cell RNA sequencing (scRNA‑seq), bulk RNA sequencing (bulk RNA‑seq) and molecular docking and verified using Western blotting. In osteosarcoma cells transfected with SOHLH1 siRNAs or a negative control sequence, the effects of PP7 treatment (5 μmol/L) on cell migration, invasion, ferroptosis, reactive oxygen species (ROS) production and lipid peroxidation (LPO) were analyzed. RESULTS: PP7 was identified as one of the major active constituents of Paris polyphylla. In the tumor-bearing mice, PP7 treatment significantly lower the tumor volume and mass. In 143B and HOS cells, PP7 concentration‑dependently inhibited cell proliferation, and at 5 μmol/L, PP7 significantly inhibited cell proliferation, migration and invasion. Multi‑omics analysis identified SOHLH1 as a potential target of PP7, and Western blotting confirmed that PP7 upregulated SOHLH1 expressions at both the mRNA and protein levels. SOHLH1 silencing obviously attenuated the inhibitory effects of PP7 on cell migration and invasion and reduced PP7‑induced ferroptosis. CONCLUSIONS: PP7 suppresses osteosarcoma xenograft growth in mice by inducing ferroptosis via upregulating SOHLH1 expression.
[Analysis of setup errors and their correlation with clinical factors in image-guided radiotherapy for prostate cancer using different immobilization devices].
Guo X, Liu Y, Xiong Y … +3 more , Liu B, Song T, Li Y
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429625 · Full text
OBJECTIVES: To quantitatively analyze setup errors of 4 immobilization devices in precision radiotherapy for prostate cancer, their accuracy differences, and the factors affecting their setup precisions. METHODS: We cond...
OBJECTIVES: To quantitatively analyze setup errors of 4 immobilization devices in precision radiotherapy for prostate cancer, their accuracy differences, and the factors affecting their setup precisions. METHODS: We conducted a retrospective analysis of 240 prostate cancer patients undergoing image-guided radiotherapy at Sun Yat-sen University Cancer Center from May, 2016 to May, 2024. According to the immobilization devices used, the patients were divided into 1.2 m vacuum bag group (=60), 1.8 m vacuum bag group (=60), Orfit frame group (=60), and customized prone board group (=60). All the patients received pre-treatment cone-beam CT (CBCT) scans, and setup errors in the right-left (RL), superior-inferior (SI), and anterior-posterior (AP) directions were obtained through XVI system grayscale registration. Further subgroup analyses were performed based on patient stratifications by lymph node irradiation status (=120 each), age (<65 years, =80; ≥65 years, =160), and BMI (BMI<24 kg/m², =120; BMI≥24 kg/m², =120). RESULTS: The setup errors differed significantly among the 4 groups in three-dimensional directions (<0.05). The customized prone board group showed minimal errors in the RL (0.02±0.25 cm) and SI (0.01±0.32 cm) directions, but demonstrated the largest error in the AP direction (-0.28±0.36 cm). The patients with lymph node irradiation had significantly greater AP directional errors (-0.22±0.36 cm) than those without (-0.01±0.43 cm; <0.001). BMI showed a negative correlation with SI directional errors (=-0.45, P<0.001), while age was not significantly correlated with the setup errors (>0.05). CONCLUSIONS: The customized prone board demonstrates clinically significant advantages for its high setup accuracies in RL and SI directions in spite of its systematic AP directional errors. The setup accuracy in the SI direction is especially important for patients with lymph node irradiation or low BMI. Our findings provide quantitative evidence for immobilization device selection and individualized optimization of precision radiotherapy for prostate cancer.
[ResLSTM-TemporalSE: an automated classification model for multi-lead ECG signals].
Qu M, Fu R
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429624 · Full text
OBJECTIVES: We propose an efficient deep learning model to improve the classification accuracy in automatic classification tasks of 12-lead electrocardiogram (ECG) signals. METHODS: We designed a new ResLSTM-TemporalSE n...
OBJECTIVES: We propose an efficient deep learning model to improve the classification accuracy in automatic classification tasks of 12-lead electrocardiogram (ECG) signals. METHODS: We designed a new ResLSTM-TemporalSE network architecture by incorporating a multi-layer Residual Long Short-Term Memory (ResLSTM) structure and introducing skip connections between LSTM layers to establish residual learning pathways for the temporal features. A temporal attention mechanism was integrated into the traditional Squeeze-and-Excitation (SE) module to enhance channel-wise feature representation while capturing long-term temporal dependencies within ECG signals, thereby an efficient hierarchical feature extraction framework was constructed. The model was validated using the public CPSC2018 dataset and a private clinical dataset from the Seventh Affiliated Hospital of Southern Medical University. RESULTS: The experimental results demonstrated that the model achieved a classification accuracy of 99.70% on the CPSC2018 test set, with precision, recall, and F1-score values of 0.9966, 0.9370, and 0.9653, respectively. On the private clinical dataset, it attained an accuracy of 82.77%, with precision, recall, and F1-score values of 0.6811, 0.8961, and 0.7723. Ablation studies confirmed the significant contributions of both the residual connections and the temporal attention module to model performance. CONCLUSIONS: The ResLSTM-TemporalSE model effectively integrates spatiotemporal features of the ECG signals and demonstrates superior classification performance on the CPSC2018 benchmark while maintaining strong generalization capabilities in real-world clinical settings. This framework provides a robust solution for automated ECG analysis and holds significant promise for clinical applications.
[Helicid alleviates depression-like behavior in rats with chronic unpredictable mild stress through the NCALD/sGC/cGMP/PKG axis].
DU X, Zhang X, Lu J … +6 more , Ge P, Hu H, Fu M, Zhang Y, Wang G, Tong J
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429623 · Full text
OBJECTIVES: To investigate the molecular mechanism of helicid for improving depressive-like behaviors in rats exposed to chronic unpredictable mild stress (CUMS). METHODS: SD rats were randomly divided into normal contro...
OBJECTIVES: To investigate the molecular mechanism of helicid for improving depressive-like behaviors in rats exposed to chronic unpredictable mild stress (CUMS). METHODS: SD rats were randomly divided into normal control group (=20) and CUMS group (=70) to receive no stimulation and mild unpredictable stress for 6 weeks, respectively. After successful modeling, CUMS rats were further divided into 7 subgroups for intracerebroventricular injection with saline, adeno-associated virus (AAV) vector, or AAV carrying si-NCALD (NCALD silencing experiment, =10); or intracerebroventricular injection with saline, saline with daily helicid gavage, AAV vector with helicid gavage, or NCALD-overexpressing AAV with helicid gavage (NCALD overexpresison experiment, =10). The depressive state of the rats was evaluated by assessing changes in body weight, sucrose preference, and open field test. The expressions of NCALD, sGCα1, sGCβ1, PKG1/2, and cleaved-caspase 3 in the hippocampus of the rats were detected by Western blotting, and hippocampal cGMP level was determined with ELISA. RESULTS: Compared with the normal control rats, CUMS rats showed significantly increased hippocampal expressions of NCALD and cleaved caspase-3 and abnormal activation of the sGC/cGMP/PKG pathway. Silencing NCALD by intracerebroventricular injection of AAV-si-NCALD significantly reduced cleaved caspase-3 and inhibited sGC/cGMP/PKG pathway activation in the hippocampus, and improved depressive-like behaviors of the rats. Helicid treatment produced similar effects, but its effect was abolished by intracerebroventricular injection of NCALD-overex-pressing AAV. CONCLUSIONS: Helicid relieves depressive-like behaviors in CUMS rats by downregulating NCALD, inhibiting abnormal sGC/cGMP/PKG activation, and reducing hippocampal apoptosis.
[Resveratrol protects barrier function of mouse brain microvascular endothelial cell monolayers with oxygen/glucose deprivation and PM exposure by maintaining mitochondrial dynamics balance].
Qin M, Sun S, Liu J … +7 more , Gao Y, Wang H, Wang Y, Sun A, Yan J, Wang J, Yu Y
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429622 · Full text
OBJECTIVES: To evaluate the effect of resveratrol (RES) on barrier function of mouse brain microvascular endothelial cell monolayers exposed to oxygen/glucose deprivation/reoxygenation (OGD/R) and PM and explore the role...
OBJECTIVES: To evaluate the effect of resveratrol (RES) on barrier function of mouse brain microvascular endothelial cell monolayers exposed to oxygen/glucose deprivation/reoxygenation (OGD/R) and PM and explore the role of mitochondrial fission and fusion in protecting endothelial barrier function. METHODS: Cultured mouse brain microvascular endothelial cells were exposed to OGD/R, treated with PM (100 μg/mL) before OGD/R, or pretreated with RES (40 mg/mL) prior to OGD/R+PM exposures. The changes in cell viability were examined with CCK-8 assay, and cell permeability was assessed by measuring transendothelial electrical resistance (TEER) and FITC-dextran permeation. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured, and intracellular and mitochondrial ROS levels were detected using fluorescent probes. Mitochondrial morphology in the treated cells was observed using Mito-Tracker Red CMXRos. Western blotting was performed to detect the changes in cellular expressions of the tight junction proteins (ZO-1, occludin, and claudin-5) and mitochondrial dynamics-associated proteins (Drp1, Fis1, Mfn2, and OPA1). RESULTS: Compared with the normal control cells, the cells exposed to OGD/R or both OGD/R and PM showed significantly decreased TEER levels, increased permeability, elevated oxidative stress, and increased ROS fluorescence intensities. Obvious mitochondrial fragmentation and morphological changes in the mitochondria were observed in the exposed cells, which also showed decreased expressions of tight junction proteins and mitochondrial fusion proteins with increased expressions of mitochondrial fission proteins. RES pretreatment of the endothelial cells before the exposures significantly reduced membrane permeability, lowered ROS levels, improved mitochondrial morphology, increased expressions of tight junction and fusion proteins, and decreased fission protein expressions. CONCLUSIONS: RES can protect barrier function of mouse brain microvascular endothelial cell monolayers exposed to OGD/R and PM by modulating mitochondrial dynamics, potentially through promoting mitochondrial fusion and inhibiting mitochondrial fission.
[Indole-3-acetic acid alleviates -induced pyroptosis in cerebral microvascular endothelial cells by regulating stress granule-mediated NLRP3 inflammasome activation].
Chen J, Zou J, Zhou B … +3 more , Gao X, Huang P, Cao H
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429621 · Full text
OBJECTIVES: To investigate whether indole-3-acetic acid (IAA) alleviates (Cn)‑induced pyroptosis in cerebral microvascular endothelial cells by modulating stress granules (SGs) formation and the NLRP3 inflammasome. METH...
OBJECTIVES: To investigate whether indole-3-acetic acid (IAA) alleviates (Cn)‑induced pyroptosis in cerebral microvascular endothelial cells by modulating stress granules (SGs) formation and the NLRP3 inflammasome. METHODS: cultured cerebral microvascular endothelial cells were pretreated with different concentrations of IAA before Cn infection (10⁷/mL), and the changes in cellular expresisons of G3BP1, DDX3X, NLRP3 and pyroptosis-related proteins, cytokines, and cell viability were deceted using Western blotting, immunofluorescence staining, ELISA, and CCK-8 assay. In the animal experiment, C57BL/6 mice with cyclophosphamide-induced immunosuppression were pretreated with saline or IAA gavage for 7 days before intravenous Cn injection. The changes in blood-brain barrier (BBB) integrity of the mice was assessed with Evans blue assay, and the brain cortical tissues were analyzed for changes in protein expressions. RESULTS: Cn infection significantly downregulated G3BP1 expression and upregulated the expressions of DDX3X and NLRP3 in cultured cerebral microvascular endothelial cells. IAA intervention not only restored normal expressions of G3BP1, DDX3X, and NLRP3, but also effectively suppressed the activation of pyroptosis-related proteins, including NT-GSDMD/GSDMD and P20/caspase-1, and reduced the release of IL-18 and IL-1β. IAA treatment also inhibited the translocation of DDX3X to NLRP3 induced by Cn infection and promoted the binding between DDX3X and G3BP1. In Cn-infected C57BL/6 mice, IAA treatment significantly alleviated BBB injury, decreased the expression of ZO-1 in the cerebral cortex, and effectively ameliorated abnormal expressions of VEGFR2, G3BP1, DDX3X, NLRP3, NT-GSDMD/GSDMD and P20/caspase-1. CONCLUSIONS: IAA effectively alleviates Cn infection-induced pyroptosis of cerebral microvascular endothelial cells by modulating the formation of SGs and activating the NLRP3 inflammasome.
[ Decoction alleviates non-alcoholic fatty liver disease in rats by activating the AMPK/m-TOR signaling pathway and reducing lipid synthesis].
Shang D, Li W, Cui L … +1 more , Chen M
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429620 · Full text
OBJECTIVES: To explore therapeutic mechanism of ( Decoction, HGT) for alleviating non-alcoholic fatty liver disease (NAFLD) in rats. METHODS: Network pharmacology analysis was used to predict the active components of HG...
OBJECTIVES: To explore therapeutic mechanism of ( Decoction, HGT) for alleviating non-alcoholic fatty liver disease (NAFLD) in rats. METHODS: Network pharmacology analysis was used to predict the active components of HGT against NAFLD and their potential targets, and the core targets were identified using the protein-protein interaction network, followed by GO and KEGG pathway enrichment analyses. A rat model of high-fat diet (HFD)-induced NAFLD was used to test the effects of saline, silymarin, and low-, moderate-, and high-dose HGT on serum levels of ALT, AST, LDL, LDH, TG and TC, liver histopathology, and protein and mRNA expressions of ACC1, FASN, AMPK and m-TOR. In free fatty acid (FFA)-induced HepG2 cells, the effects of blank and HGT-medicated sera, compound C (an AMPK inhibitor), and MHY1485 (a mTOR agonist) were tested on cell viability, intracellular lipid deposition, TC and TG levels, and expressions of ACC1, FASN, AMPK and m-TOR. RESULTS: We identified 130 active components in HGT, 267 common targets with NAFLD, and 53 core gene nodes, nearly half of which were involved in lipid metabolism. HGT treatment of NAFLD was closely associated with lipid and atherosclerosis signaling, insulin resistance signaling, and AMPK signaling. In rat models of NAFLD, HGT significantly alleviated liver injury and lipid accumulation, and suppressed mRNA and protein expressions of ACC1 and FASN. In FFA-induced HepG2 cells, HGT-medicated serum obviously reduced TG and TC levels and inhibited ACC1 and FASN mRNA and protein expressions. The results of and experiments both demonstrated that HGT activated the AMPK/mTOR signaling pathway by promoting p-AMPK expression and suppressing p-mTOR expression, and its regulatory effects on p-AMPK, p-mTOR, ACC1, and FASN were differentially modulated by compound C and MHY1485. CONCLUSIONS: HGT alleviates NAFLD in rats by activating the AMPK/m-TOR signaling pathway and reducing lipid synthesis.
[Dietary secoisolariciresinol diglucoside alleviates chronic kidney disease in offspring rats caused by maternal trans-fatty acid exposure by regulating the Bcl-2/Bax/caspase-3 signaling axis].
Ma S, Chen M, Wu T … +1 more , Zhao W
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429619 · Full text
OBJECTIVES: To investigate the potential mechanism underlying the protective effect of secoisolariciresinol diglucoside (SDG) against chronic kidney disease (CKD) in offspring mice caused by maternal exposure to trans fa...
OBJECTIVES: To investigate the potential mechanism underlying the protective effect of secoisolariciresinol diglucoside (SDG) against chronic kidney disease (CKD) in offspring mice caused by maternal exposure to trans fatty acids (TFA) during pregnancy and lactation. METHODS: Thirty female C57BL/6 mice were randomized into control group, TFA model group, and 3 TFA model groups treated with SDG at low, medium and high doses (10, 20 and 30 mg/kg, respectively). The changes in blood urea nitrogen (BUN) and serum creatinine (CRE) levels of the mice were measured. Network pharmacology analysis was conducted to explore protective mechanism of SDG against TFA-induced renal injury, and molecular docking was used to assess the binding affinity of SDG to Bcl-2, Bax, and caspase-3. The protein expressions of cleaved caspase-3, Bax, and Bcl-2 in the renal tissues of the offspring mice were detected with Western blotting. RESULTS: The mice in TFA group showed significantly higher BUN and CRE levels than those in the control group. Treatment with SDG at the medium and high doses significantly reduced BUN and CRE levels in the mouse models. Network pharmacology and molecular docking suggested that SDG ameliorated renal injury by targeting the apoptosis-related Bcl-2/Bax/caspase-3 axis. The results of Western blotting showed the mouse models in TFA exposure group had increased renal cell apoptosis with elevated expression levels of cleaved caspase-3 protein and a decreased Bcl-2/Bax ratio (<0.05), and intervention with SDG at all the 3 doses significantly reduced renal cell apoptosis and renal expression of cleaved caspase-3 and increased the Bcl-2/Bax ratio in the mouse models. CONCLUSIONS: Maternal TFA exposure during gestation and lactation induces renal injury in offspring mice. Dietary SDG intervention can mitigate TFA-induced renal injury in offspring mice possibly by suppressing renal cell apoptosis via regulating the Bcl-2/Bax/caspase-3 signaling axis.
[ Granules ameliorate cancer-related fatigue during breast cancer chemotherapy by regulating the AKT1/BAD/BCL-2 pathway].
Sun X, Wang K, Wang G … +4 more , Dai Q, Chen J, Kong X, Luan J
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429618 · Full text
OBJECTIVES: To explore the therapeutic mechanism of (FZXY) Granules for relieving cancer-related fatigue (CRF) during chemotherapy in breast cancer patients based on the traditional Chinese medicine (TCM) theory of "" (...
OBJECTIVES: To explore the therapeutic mechanism of (FZXY) Granules for relieving cancer-related fatigue (CRF) during chemotherapy in breast cancer patients based on the traditional Chinese medicine (TCM) theory of "" (supporting healthy and eliminating pathogens). METHODS: Ninety CRF patients with breast cancer and syndrome were randomized equally into control group with chemotherapy and symptomatic treatment and study group with additional treatment with FZXY Granules, and their Piper Fatigue Scale (PFS), Karnofsky Performance Status (KPS), and TCM syndrome scores were compared. Network pharmacology analysis was used to identify the active components in FZXY Granules, the drug targets, and disease-related targets. Protein-protein interaction (PPI) network was constructed followed by enrichment analysis. Molecular docking study was conducted to explore the interactions between quercetin and the core targets. In a CRF mouse model bearing breast cancer xenograft, the effects of saline and FZXY Granule gavage were observed by assessing motor function, expressions of AKT1, p-AKT1, BCL-2, and BAD in the gastrocnemius muscle, and serum levels of IL-6 and IL-1β. RESULTS: The patients receiving FZXY Granules treatment showed significantly improved PFS, KPS, and TCM syndrome scores compared with the baseline levels and those in the control group (<0.05). Fifty-seven overlapping drug-disease targets were screened, and 5 core targets were identified. Quercetin exhibited strong binding to AKT1 and acted likely via the apoptosis pathways. In the CRF mouse models, FZXY Granules obviously improved motor function of the mice, reversed abnormal apoptosis-related protein expressions in the gastrocnemius muscle, and reduced serum IL-6 and IL-1β levels. CONCLUSIONS: FZXY Granules alleviate CRF and improve TCM symptoms and quality of life of breast cancer patients during chemotherapy possibly by suppressing skeletal muscle cell apoptosis via regulating the AKT1/BAD/BCL-2 pathway and reducing IL-6 and IL-1β levels.
[Development and validation of a risk prediction model for cognitive impairment in rural elderly Chinese populations: evidence from the CHARLS study].
Wang F, Li W, Shang X … +1 more , Li F
Nan Fang Yi Ke Da Xue Xue Bao · 2025 Dec · PMID 41429617 · Full text
OBJECTIVES: To develop and validate a risk prediction model for cognitive impairment in community-dwelling elderly individuals in China. METHODS: This cross-sectional study was based on data from the 2011 China Health an...
OBJECTIVES: To develop and validate a risk prediction model for cognitive impairment in community-dwelling elderly individuals in China. METHODS: This cross-sectional study was based on data from the 2011 China Health and Retirement Longitudinal Study (CHARLS), and the data of 2228 individuals aged ≥60 years were analyzed. The participants were randomly divided into a training set (=1560) and an internal validation set (=668) in a 7∶3 ratio. Thirty-eight candidate variables were collected, covering sociodemographic characteristics, lifestyle and behavioral habits, chronic disease history, physical function, and self-rated health status. Feature selection was performed using the least absolute shrinkage and selection operator (LASSO) regression, followed by multivariate logistic regression to identify independent risk factors for cognitive impairment. A nomogram was constructed based on these factors, its discrimination power and calibration were assessed using the receiver operating characteristic (ROC) curve and calibration plot, respectively, and its clinical utility was evaluated using decision curve analysis (DCA). RESULTS: Age, years of education, alcohol consumption, systolic blood pressure, grip strength, and depressive symptoms were identified as independent predictors of cognitive impairment in Chinese elderly individuals. The area under the ROC curve of the constructed nomogram was 0.839 (95% : 0.814-0.864) in the training set and 0.840 (95% C: 0.801-0.879) in the validation set, indicating good predictive performance of the model. The calibration plots demonstrated good agreement between the predicted and observed outcomes, and the DCA showed good clinical utility of the model. CONCLUSIONS: The nomogram developed in this study based on LASSO-selected predictors demonstrates high accuracy, discrimination power, and potential clinical applicability to facilitate early identification and intervention of cognitive impairment among rural elderly individuals in China.
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