Nan Fang Yi Ke Da Xue Xue Bao = Journal Of Southern Medical University[JOURNAL]
Sun
200 papers
[Intravenous dexamethasone enhances efficacy of brachial plexus block the costoclavicular space: a randomized, double-blind, single-center trial].
Wang S, Wu M, Sun N … +6 more , Lin C, Chen Y, Zhang C, Deng F, Ma X, Fang H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198965 · Full text
OBJECTIVES: To investigate the effect of intravenous 8 mg dexamethasone injection on the efficacy of ultrasound-guided brachial plexus block (BPB) with 20 mL 0.375% ropivacaine the costoclavicular space (CCS). METHODS:...
OBJECTIVES: To investigate the effect of intravenous 8 mg dexamethasone injection on the efficacy of ultrasound-guided brachial plexus block (BPB) with 20 mL 0.375% ropivacaine the costoclavicular space (CCS). METHODS: Eighty-four patients (18-65 years, ASA I-II, and BMI 18-25 kg/m²) undergoing elective surgery below the elbow were randomized into two groups to receive ultrasound-guided BPB with 20 mL 0.375% ropivacaine the CCS combined with intravenous injection of 8 mg (4 mL) dexamethasone (trial group) or 4 mL normal saline (control group). The mean arterial pressure (MAP) and heart rate (HR) were measured before block, at the end of block, and at the start of surgery, and the type of surgery, duration of surgery, and block onset time (T1) were recorded. After the operation, the patients were followed up for durations of sensory (T2) and motor (T3) block, patient's satisfaction with anesthesia, incidences of nausea and vomiting within 24 h, and incidences of nerve block-related adverse effects within one week. RESULTS: No significant difference in block onset time was found between the two groups (>0.05). The patients in the trial group exhibited significantly prolonged T2 and T3 (<0.001) with higher anesthesia satisfaction (<0.05). No significant differences were observed in postoperative adverse events between the two groups (>0.05). CONCLUSIONS: Intravenous 8 mg dexamethasone, which does not affect block onset time of BPB the CCS, significantly prolongs the sensory and motor block durations and improves anesthesia satisfaction without significantly increasing the incidences of postoperative adverse events.
[Myricetin inhibits proliferation and migration of bladder cancer cells by inhibiting HSP90AA1-mediated AKT phosphorylation].
Sun R, Li Y, Zuo L … +3 more , Tao J, Dong X, Liu H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198964 · Full text
OBJECTIVES: To explore the targets and molecular mechanisms mediating the inhibitory effect of myricetin against bladder cancer. METHODS: The potential targets of myricetin were predicted using SwissTargetPrediction and...
OBJECTIVES: To explore the targets and molecular mechanisms mediating the inhibitory effect of myricetin against bladder cancer. METHODS: The potential targets of myricetin were predicted using SwissTargetPrediction and SEA Search Server, bladder cancer-related targets were screened from TCGA transcriptome and FinnGen plasma proteome data, and the intersecting genes were obtained to identify the potential targets. A protein-protein interaction network was constructed, followed by GO and KEGG enrichment analyses. Molecular docking and dynamics simulations were performed to validate the binding between myricetin and the core targets. Amino acid residue virtual mutation was conducted to confirm the binding specificity of myricetin to HSP90AA1. Public single-cell transcriptomic and CRISPR screening data were analyzed to evaluate the cell-type specificity and functional essentiality of HSP90AA1. UM-UC-3 cells were used to examine the effects of myricetin on cell proliferation and migration and expressions of HSP90AA1 and PI3K-AKT pathway proteins. RESULTS: Thirty potential targets of myricetin against bladder cancer were obtained, and HSP90AA1 was identified as the central target. KEGG analysis indicated significant enrichment of the target genes in the PI3K-AKT signaling pathway. Molecular docking and dynamics simulations demonstrated high binding affinity and stable conformation between myricetin and HSP90AA1. Bioinformatics analysis suggested that HSP90AA1 was highly and specifically expressed in bladder cancer urothelial cells, and its high expression was correlated with poor progression-free survival of the patients. In UM-UC-3 cells, myricetin concentration-dependently inhibited cell proliferation and migration, and downregulated mRNA level of HSP90AA1 and protein expressions of HSP90AA1, p-PI3K, and p-AKT. CONCLUSIONS: Myricetin inhibits bladder cancer cell proliferation and migration possibly by targeting HSP90AA1 and regulating the PI3K-AKT signaling pathway, suggesting its potential as a therapeutic agent for bladder cancer.
[ Granules attenuate cartilage injury in knee osteoarthritis patients with liver-kidney deficiency syndrome by regulating the Nrf2 pathway].
Cheng Y, Huang C, Zhang J … +2 more , Zhu Y, Qian A
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198963 · Full text
OBJECTIVES: To explore the mechanism mediating the ameliorative effect of Granules on cartilage injury in knee osteoarthritis (KOA). METHODS: Bioinformatics approaches were used for analyzing the active ingredients of...
OBJECTIVES: To explore the mechanism mediating the ameliorative effect of Granules on cartilage injury in knee osteoarthritis (KOA). METHODS: Bioinformatics approaches were used for analyzing the active ingredients of Granules, their potential targets, the KOA- and ferroptosis-related genes, and their intersection genes. A compound-ingredient-disease-target network and the protein-protein interaction (PPI) network were constructed to identify the key active ingredients and core targets, which were verified by molecular docking studies. In the clinical trial, 62 KOA patients were randomly assigned into the observation group and control group (=31) for treatment with glucosamine hydrochloride tablets and additional Granules for 12 weeks, respectively, with 20 healthy participants serving as the healthy control group. Serum levels of cartilage injury markers (MMP-13, CTX-II, and COMP) and ferroptosis-related indices (GPX4, ACSL4, 4-HNE, and Fe) were measured using ELISA, and expressions of Keap1, Nrf2, SLC7A11, HO-1, and GPX4 mRNAs were determined with real-time PCR. RESULTS: Four key active ingredients (quercetin, eupatilin, kaempferol, and wogonin) of Granules and 5 core targets (AKT1, TP53, IL-6, JUN, and Nrf2) were identified, which were involved in cancer, AGE-RAGE signaling, and the NFE2L2 (Nrf2) signaling pathways. Molecular docking showed strong binding between the active compounds and their targets, with NFE2L2 exhibiting the highest binding affinity. Compared with the control patients, KOA patients treated with Granules showed significantly upregulated Nrf2, SLC7A11, HO-1, and GPX4 mRNA expressions (<0.05), downregulated Keap1 expression (<0.05), reduced serum levels of MMP-13, CTX-II, COMP, ACSL4, 4-HNE, and Fe (<0.05), and increased GPX4 level (<0.05). CONCLUSIONS: Granules alleviate KOA through its key active ingredients quercetin and eupatilin, which activate the Nrf2 signaling pathway to modulate ferroptosis by targeting NFE2L2 and other therapeutic targets, suggesting a multi-component, multi-target, and multi-pathway synergistic mechanism for ameliorating chondrocyte injury in KOA.
[miR-143-3p alleviates neuropathic pain in mice with spared nerve injury by targeting the KRAS/RalA pathway and inhibiting astrocyte activation].
Lin Y, Yao J, Chen Y … +1 more , Qin Z
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198962 · Full text
OBJECTIVES: To investigate the therapeutic effect of microRNA (miR-143-3p) on neuropathic pain in mice and clarify its target gene and molecular mechanism. METHODS: Spared nerve injury (SNI) models were established in 8-...
OBJECTIVES: To investigate the therapeutic effect of microRNA (miR-143-3p) on neuropathic pain in mice and clarify its target gene and molecular mechanism. METHODS: Spared nerve injury (SNI) models were established in 8-week-old male C57BL/6J mice, with sham-operated mice as the control group (=6). The treatment group received a single intrathecal injection of miR-143-3p agomir on day 7 after SNI modeling, and in KRAS agonist group, KRA-533 was intrathecally injected on day 8 following miR-143-3p agomir injection. Mechanical withdrawal thresholds of the ipsilateral paw of the mice were measured using von Frey filaments. Bioinformatics analyses were used to explore the potential targets and signaling pathways. In a C8-D1A astrocyte model of lipopolysaccharide (LPS)-induced inflammation, the effect of miR-143-3p mimic and KRA-533 on the expressions of the identified targets were detected using qRT-PCR and Western blotting. Spinal morphology in the mouse models and proliferative activity of C8-D1A cells were observed with immunofluorescence staining, and the levels of pro-inflammatory factors were determined with enzyme-linked immunosorbent assay (ELISA). RESULTS: miR-143-3p agomir significantly increased mechanical withdrawal thresholds of SNI mice, and the effect lasted nearly 3 weeks. KRAS was identified as a direct target of miR-143-3p. In SNI mouse models, miR-143-3p significantly inhibited KRAS expression, RalA/TBK1/NF-κB signaling pathway activation, and astrocyte activation, and upregulated the levels of IL-6, IL-1β, and TNF-α. The KRAS agonist KRA-533 significantly reversed the analgesic effect of miR-143-3p and its inhibitory effects on downstream pathway activation, astrocyte activation, and neuroinflammation. In C8-D1A cells, overexpression of miR-143-3p effectively suppressed LPS-induced noncanonical Ras pathway activation and inhibited cell proliferation and inflammatory response, which were reversed by treatment with KRA-533. CONCLUSIONS: miR-143-3p overexpression alleviates neuropathic pain in mice by targeting KRAS to regulate the noncanonical Ras pathway and inhibiting astrocyte activation and neuroinflammation, suggesting a new strategy for clinical treatment of SNI.
[Ultrafine powder alleviates lipopolysaccharide-induced acute lung injury in mice by suppressing ferroptosis and modulating the NF-κB/STAT3 signaling axis].
Zhu J, Shao N, Huang Z … +6 more , Liu Y, Meng X, Liu Z, Sun Y, Dong J, Fan H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198961 · Full text
OBJECTIVES: To investigate the protective effects of ultrafine powder (UXP) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the underlying mechanism. METHODS: Fifty-four male C57BL/6 mice we...
OBJECTIVES: To investigate the protective effects of ultrafine powder (UXP) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the underlying mechanism. METHODS: Fifty-four male C57BL/6 mice were randomized into 9 groups, including a control group and 8 intratracheal LPS instillation-induced ALI model groups gavaged with saline, dexamethasone (DEX, 1 mg/kg), or 100, 250, or 500 mg/kg UXP or granule powder (=6) for 6 consecutive days, starting on the day of modeling. After the treatment, the lung wet-to-dry (W/D) ratios were determined, inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were measured by ELISA, and inflammatory cell infiltration was assessed by flow cytometry. Histopathological injury of the lungs was observed using HE staining, and pulmonary SOD, MDA, and GSH levels were determined. Pulmonary mRNA expressions of inflammatory mediators were quantified by RT-qPCR, and NF‑κB and STAT3 activation was analyzed using Western blotting; mitochondrial ultrastructure was examined with transmission electron microscopy. In a LPS-stimulated BEAS-2B cell model, the effects of UXP and DEX were assessed on cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial function, lipid peroxidation, and ferrous iron levels. RESULTS: The LPS-challenged mice exhibited a higher lung W/D ratio and increased BALF cytokine levels and inflammatory cell counts with pronounced lung inflammation and tissue damage, lowered SOD and GSH levels, elevated MDA levels, increased mRNA expressions of inflammatory mediators and the p-NF‑κB/NF‑κB and p-STAT3/STAT3 ratios, and obvious mitochondrial damages. UXP markedly alleviated these changes with an efficacy comparable to DEX. In LPS-stimulated BEAS-2B cells, UXP significantly improved cell viability, redcued cell apoptosis and ROS accumulation, preserved mitochondrial integrity, and reduced lipid peroxidation and ferroptosis-associated changes. CONCLUSIONS: UXP has strong protective effects against LPS-induced ALI in mice possibly by suppressing inflammation, oxidative stress, ferroptosis, and apoptosis, modulating the NF‑κB/STAT3 signaling axis, and maintaining mitochondrial integrity.
[KLF10 overexpression alleviates neuroinflammation and anxiety-depressive disorder in rats by downregulating the NF-κB/NLRP3 pathway].
Liu A, Guo W, Li J … +2 more , Zhang T, Xu D
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198960 · Full text
OBJECTIVES: To elucidate the neuroimmune regulatory mechanism of the circadian rhythm gene KLF10 as a biomarker for anxiety depressive disorder (ADD). METHODS: The differentially expressed circadian rhythm genes were scr...
OBJECTIVES: To elucidate the neuroimmune regulatory mechanism of the circadian rhythm gene KLF10 as a biomarker for anxiety depressive disorder (ADD). METHODS: The differentially expressed circadian rhythm genes were screened using human peripheral blood gene chip data from the GEO database (including 64 healthy individuals, 62 patients with major depressive disorder [MDD], and 59 with ADD) in conjunction with the MSigDB database. Weighted gene co-expression network analysis and machine learning models were employed to identify the core genes, followed by KEGG pathway enrichment analysis and evaluation of their diagnostic efficacy using ROC curves. In a male SD rat model of ADD induced by chronic restraint and corticosterone stress, the changes in depressive-like behaviors, hippocampal and amygdala pathologies, levels of inflammatory and pro-inflammatory cytokines, co-localization of KLF10 and p-p65 expression, and expression levels of NF‑κB/NLRP3 pathway molecules were examined following stereotactic AAV virus injection into the lateral ventricle for KLF10 overexpression. RESULTS: Compared with healthy individuals, the depressive patients showed differential expressions of 9 circadian rhythm genes. Compared with the MDD patients, the patients with ADD had significantly higher immune infiltration scores with upregulated NOD-like receptor and NF‑κB signaling pathways. The specific biomarker KLF10 demonstrated a diagnostic efficacy of 0.885. In the rat models of AOD, KLF10 overexpression significantly ameliorated depression- and anxiety-like behaviors, restored the balance between the pro- and anti-inflammatory cytokines, and improved hippocampal and amygdala pathologies. KLF10 overexpression also markedly upregulated NFKBIA mRNA, downregulated NLRP3 and RELA mRNAs, and reduced protein expressions of p-IκB‑α, p-p65, and NLRP3 in the brain tissues of the rats. CONCLUSIONS: KLF10 overexpression ameliorates ADD behaviors in rats by inhibiting hippocampal-amygdala inflammation downregulating the NF‑κB/NLRP3 pathway, suggesting the potential of KLF10 as a diagnostic biomarker and therapeutic target for AOD.
[Multi-omics integration deciphers immune-metabolic heterogeneity in colorectal cancer: a prognostic model and therapeutic strategies targeting ANGPTL4/FABP4/RBP7].
Ding N, Peng T, Mo L … +7 more , Hu X, Yang Z, Xiao Y, Fu X, Zhao J, Li L, Zhang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198959 · Full text
OBJECTIVES: To explore the heterogeneity of tumor immune microenvironment (TIME) in colorectal cancer (CRC) and the resultant treatment resistance and develop a prognostic model for predicting the treatment outcomes of C...
OBJECTIVES: To explore the heterogeneity of tumor immune microenvironment (TIME) in colorectal cancer (CRC) and the resultant treatment resistance and develop a prognostic model for predicting the treatment outcomes of CRC. METHODS: The multi-omics data including transcriptomic, somatic mutation and single-cell RNA sequencing data of a total of 1136 CRC samples from a TCGA cohort (=568) and a GEO cohort (=568) were integrated. The TCGA cohort was divided into Immunity_High and Immunity_Low subtypes by single-sample gene set enrichment analysis (ssGSEA) and t-SNE algorithm. A prognostic model was constructed using univariate Cox regression combined with LASSO-Cox regression, and the functions of the core genes including ANGPTL4, FABP4 and RBP7 were verified by single cell RNA-seq, molecular docking, kinetic simulations and qPCR/IHC experiments. RESULTS: The Immunity_High subtype of CRC was enriched with CD8 T cells and had significantly longer patient survival, while the Immunity_Low subtype was characterized by M0 macrophage infiltration. The prognostic model constructed based on 12 genes including ANGPTL4, FABP4 and RBP7 showed good predictive performance, with the AUC of 3-year survival rate reaching 0.765, an overall AUC of 0.76 in the TCGA cohort, and an overall AUC of 0.70 in the GEO cohort. Mechanistically, ANGPTL4 regulated macrophage polarization, FABP4 mediated fibroblast reprogramming, and RBP7 up-regulated PD-L1 expression. Molecular docking and kinetic simulations confirmed stable binding of retinoic acid and rosiglitazone to the core targets with the minimum binding energy of -8.3 kcal/mol. CONCLUSIONS: The constructed prognostic model and the identified potential therapeutic targets provide new strategies to address immune therapy resistance for CRC.
Development and validation of a machine learning-based model for assessing coronary artery disease risk in postmenopausal women: a dual-center retrospective study.
Deng Y, Pan J, He S … +2 more , Zhou W, Zhang J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 May · PMID 42198958 · Full text
OBJECTIVES: To investigate the risk factors of coronary heart disease (CHD) and develop a risk assessment model for CHD in postmenopausal women. METHODS: General information, medical history, and laboratory test results...
OBJECTIVES: To investigate the risk factors of coronary heart disease (CHD) and develop a risk assessment model for CHD in postmenopausal women. METHODS: General information, medical history, and laboratory test results of the patients were collected from postmenopausal women with CHD admitted to two medical centers in Yangzhou (Jiangsu Province, China) from November, 2018 to November, 2023. After excluding cases with incomplete medical records, 1197 patients were included, who were divided into the training cohort (=821) and validation cohort (=376) based on the hospital of admission. In the training cohort, the risk factors for CHD in postmenopausal women were identified using Lasso regression, multivariate logistic regression analysis, and machine learning algorithms including Light GradientBoosting Machine (LGBM), Random Forest (RF), Decision Tree (DT), Support Vector Machine (SVM), Extreme Gradient Boosting (XGBoost), K-Nearest Neighbors (KNN), and Naive Bayes (NB). Risk assessment models were constructed using these algorithms, and their performance was evaluated using ROC curves, decision curve analysis (DCA), and calibration curves. RESULTS: Lasso regression suggested body mass index (BMI) classification and glycated hemoglobin were independent risk factors for CHD in postmenopausal women, whereas age at menopause and high-density lipoprotein cholesterol (HDL-C) were independent protective factors (<0.05). Among the machine learning models, XGBoost demonstrated the best assessment performance in both the training set (AUC: 0.912; sensitivity: 0.892; specificity: 0.766; recall: 0.892; F1-score: 0.899) and the validation set (AUC: 0.891; sensitivity: 0.836; specificity: 0.921; recall: 0.837; F1-score: 0.877). Calibration curve and DCA curve analyses indicated good consistency between the predicted and actual outcomes. A nomogram and SHAP summary plot were used to visualize and interpret the logistic regression model and the XGBoost model, respectively. CONCLUSIONS: The risk assessment model for CHD in Chinese postmenopausal women established in this study demonstrates good accuracy and applicability to allow early identification of high-risk patients.
[Research progress in mechanisms of dietary resistant starch for regulating glucose and lipid metabolism].
Liu K, Li X, Zhang Y … +2 more , Sun J, Liao W
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045046 · Full text
The global prevalence of metabolic diseases such as obesity, diabetes, and cardiovascular diseases is closely related to overnutrition and imbalanced dietary patterns. As an important carbohydrate, starch directly affect...
The global prevalence of metabolic diseases such as obesity, diabetes, and cardiovascular diseases is closely related to overnutrition and imbalanced dietary patterns. As an important carbohydrate, starch directly affects the homeostasis of glucose and lipid metabolism due to its digestion characteristics. Resistant starch (RS) with unique anti-digestive properties and prebiotic functions has become the current hotspot in dietary nutrition research for improving glucose and lipid metabolism disorders. This review summarizes the digestive characteristics of starch and the comprehensive effects of RS and its mechanisms for ameliorating metabolic diseases. Diets with high RS content not only optimize glucose homeostasis by delaying glucose release, the undigested fractions entering the colon also drive the metabolic regulatory network of the gut microbiota-gut-brain axis by activating the AMPK/ACC pathway to reduce fat accumulation, enhancing intestinal barrier function mediated by short-chain fatty acids (SCFAs), and promoting GLP-1/PYY neural signal transduction. These insights facilitate the design of new healthy foods and inspire new strategies for optimizing dietary nutrition and regulating glucose and lipid metabolism disorders caused by high-carbohydrate diets.
[Visual prior-guided masked image modeling enhances chest X-ray diagnostic efficacy].
Wang J, Zhang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045045 · Full text
OBJECTIVES: To develop a masked image modeling framework that integrates clinical visual priors to enhance semantic understanding and diagnostic performance on chest X-ray images. METHODS: A novel framework VP-MIM was co...
OBJECTIVES: To develop a masked image modeling framework that integrates clinical visual priors to enhance semantic understanding and diagnostic performance on chest X-ray images. METHODS: A novel framework VP-MIM was constructed by incorporating clinical visual priors into the MIM process. Eye-tracking data from radiologists were used to distinguish diagnostically relevant from irrelevant regions during the masking phase, enabling a controlled masking strategy. In the reconstruction phase, a pyramid attentive reconstruction module was developed to introduce multi-scale supervision, which was further refined by semantic-aware recalibrated gaze heatmaps to optimize feature learning. RESULTS: Experiments conducted on the RSNA Pneumonia and ChestXray-14 public datasets showed that under linear evaluation with only 2616 pre-training samples, VP-MIM achieved an AUC of 86.83 on the RSNA Pneumonia single-label classification task and a mean AUC (mAUC) of 72.82 on the ChestXray-14 multi-label classification task. In full fine-tuning experiments, VP-MIM showed strong scalability when the amount of pre-training data increased, reaching an mAUC of 85.49 on ChestXray-14, which verified good scalability and excellent performance of this model in practical diagnostic tasks. CONCLUSIONS: VP-MIM alleviates the limitations of semantic loss and insufficient multi-scale modeling in medical imaging MIM to result in improved diagnostic performance of chest X-ray.
[A Transformer-based model using laboratory indicators efficiently differentiates ovarian cancer].
Tan S, Zhuo L, Zeng M … +4 more , Huang F, Zhu J, Cai G, Zhen X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045044 · Full text
OBJECTIVES: To evaluate the diagnostic performance of a Transformer-based deep learning model that integrates real-world laboratory test indicators for differential diagnosis of ovarian cancer. METHODS: The clinical data...
OBJECTIVES: To evaluate the diagnostic performance of a Transformer-based deep learning model that integrates real-world laboratory test indicators for differential diagnosis of ovarian cancer. METHODS: The clinical data and 99 laboratory test indicators were retrospectively collected from patients with ovarian cancer and benign ovarian lesions admitted to Department of Obstetrics and Gynecology of Tongji Hospital between January 1, 2012 and April 4, 2021. A feature selection algorithm based on ANOVA F-test was used on the training set to identify 20 key features. Each case was then converted into a unified embedded vector using a tabular data Transformer. An improved stacked Transformer model was then trained to encode these feature vectors. The proposed model was compared with multiple traditional machine learning methods. The evaluation metrics included the area under the receiver operating characteristic curve (AUC), accuracy, sensitivity, and specificity. Five-fold cross-validation was performed to assess the generalization ability and robustness of the model. RESULTS: Five-fold cross-validation showed that the Transformer-based deep learning model achieved the best performance in predicting ovarian cancer with an AUC of 0.931, an accuracy of 0.813, a sensitivity of 0.833, and a specificity of 0.865. CONCLUSIONS: The proposed Transformer-based model demonstrates high accuracy and generalization capability in predicting ovarian cancer, and may thus offer a assistance in clinical diagnosis of ovarian tumors.
[Swin-ResViT network for real-time generation of high-quality localization MR images from low-quality cine-MR].
Chen B, Wang X, Zhao X … +2 more , Song T, Li Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045043 · Full text
OBJECTIVES: To obtain high-quality pre-treatment localization MR (sMR) images from dynamic cine-MR using the Swin-ResViT network for target tracking in MRgRT. METHODS: We propose a ResViT model fused with a Swin Transfor...
OBJECTIVES: To obtain high-quality pre-treatment localization MR (sMR) images from dynamic cine-MR using the Swin-ResViT network for target tracking in MRgRT. METHODS: We propose a ResViT model fused with a Swin Transformer module (Swin-ResViT) with an optimized bottleneck layer structure for enhancing feature extraction efficiency. Seventeen liver cancer patients were retrospectively enrolled from Sun Yat-sen University Cancer Center from February to July 2024, and 12 of them were assigned to the training set (using intra-treatment cine-MR and pre-treatment planning MR), with the remaining 5 patients as the test set. Image generation quality and model performance were comprehensively evaluated by quantifying the normalized root mean square error (NRMSE), peak signal-to-noise ratio (PSNR), structural similarity index (SSIM), motion marker point error, and model inference speed between sMR and reference localization MR. RESULTS: Regarding image quality, Swin-ResViT reduced NRMSE and LPIPS by 90% and 82% compared to cine-MR (<0.001), and improved PSNR, SSIM, and CNR by 157%, 79%, and 181% (<0.001), respectively. Regarding structural accuracy, the mean localization error of motion markers at the right hepatophrenic junction in the generated dynamic sMR sequences was 0.7695±0.7294 mm (<0.05). Regarding model inference speed, for a single 224×224-pixel frame, the average processing time on an NVIDIA GeForce RTX 2080 Ti GPU was 15.5 ms for Swin-ResViT as compared with 41.4 ms for the ResViT network, demonstrating a 62% reduction. CONCLUSIONS: The Swin-ResViT model can synthesize high-quality sMR from cine-MR images. This method combines computational efficiency with significant image enhancement advantages, and thus has important clinical significance for real-time MRgRT.
[ culture, expansion, and biological characterization of mesenchymal stem cells derived from neonatal rat liver].
Chi M, Li B, Wu J … +2 more , Ge J, Tang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045042 · Full text
OBJECTIVES: To isolate liver-derived mesenchymal stem cells (L-MSCs) from neonatal rats using tissue explant method combined with enzymatic digestion. METHODS: Liver tissues aseptically harvested from 1-week-old SD rats...
OBJECTIVES: To isolate liver-derived mesenchymal stem cells (L-MSCs) from neonatal rats using tissue explant method combined with enzymatic digestion. METHODS: Liver tissues aseptically harvested from 1-week-old SD rats were rinsed, minced, and digested with D-Hanks solution containing 0.1% type-II collagenase and 0.05% type-IV collagenase for 15-20 min. After filtration through a 100-mesh screen, the cells were cultured for primary L-MSC isolation. The target cells were identified by morphological observation, flow cytometric analysis of surface CD markers, and adipogenic/osteogenic differentiation assays. RESULTS: Six to eight days after primary seeding, short spindle-shaped adherent cells formed a confluent monolayer arranged in a swirling pattern. Flow cytometry of passage-4 cells showed high expressions of CD90 [(99.33±0.06)%], CD73 [(99.60±0.10)%], CD44 [(99.50±0.10)%], and CD29 [(97.60±0.17)%] with an average positive rate of (99.01±0.86)% and low expressions of CD45 [(0.87±0.12)%], CD34 [(0.95±0.22)%], and CD11b/c [(1.71±0.28)%] with an average positive rate of (1.18±0.44)%, which was significantly lower than that of CD90, CD73, CD44, and CD29 (<0.01), consistent with the immunophenotypic characteristics of MSCs. Both adipogenic and osteogenic induction tests of the cells yielded positive results. CONCLUSIONS: L-MSCs can be successfully isolated from neonatal rat liver using tissue explant method combined with enzymatic digestion.
[Scutellarin improves metabolic dysfunction-associated steatotic liver disease in rats by regulating MMP7 and LCN2].
Ma Y, Guo L, Wang J … +3 more , Xiao W, Lv Y, Fan X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045041 · Full text
OBJECTIVES: To identify the therapeutic targets and signaling pathways that mediate the therapeutic effect of scutellarin against metabolic dysfunction-associated steatotic liver disease (MASLD). METHODS: The differentia...
OBJECTIVES: To identify the therapeutic targets and signaling pathways that mediate the therapeutic effect of scutellarin against metabolic dysfunction-associated steatotic liver disease (MASLD). METHODS: The differentially expressed genes (DEGs) in liver tissues of MASLD patients and healthy individuals were obtained from the GSE89632 dataset. The potential targets of scutellarin were screened using the PharmMapper database, and a drug-target network was constructed using Cytoscape. Functional enrichment analysis was performed using GO and KEGG pathway analysis. The intersection of scutellarin's target genes and the DEGs formed the potential therapeutic (PT) genes. Protein-protein interaction (PPI) networks were constructed using STRING to identify the key therapeutic (KT) genes. Molecular docking and dynamics simulations were used to assess the drug-target relationship. In a rat model of MASLD treated with different doses of scutellarin, the changes in serum biochemical parameters and liver pathology were analyzed. RESULTS: A total of 810 DEGs and 12 PT genes were identified, and GO and KEGG analyses suggested their involvement in inflammation regulation, cytokine response, fibrosis, and metabolism. In the rat models of MASLD, treatment with scutellarin significantly improved insulin resistance, liver function, lipid levels, inflammation, and hepatic pathology in a dose-dependent manner, and high-dose scutellarin produced better therapeutic effects than simvastatin. Scutellarin treatment significantly upregulated MMP7 and downregulated LCN2 expression in the mouse livers. CONCLUSIONS: Scutellarin ameliorates MASLD in rats possibly by modulating hepatic MMP7 and LCN2 expressions.
[Electroacupuncture at Baihui and Zusanli improves fear memory extinction in single prolonged stress mice by activating hippocampal astrocytes].
Chen X, Liu C, Yang S … +5 more , Wang J, Cheng P, Yin H, Wang J, Zhu G
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045040 · Full text
OBJECTIVES: To explore the effect of electroacupuncture (EA) on fear memory extinction in single prolonged stress (SPS) mice and the potential mechanism involving astrocytes. METHODS: Thirty-six male C57BL/6J mice were r...
OBJECTIVES: To explore the effect of electroacupuncture (EA) on fear memory extinction in single prolonged stress (SPS) mice and the potential mechanism involving astrocytes. METHODS: Thirty-six male C57BL/6J mice were randomly divided into the control, SPS model, EA treatment, paroxetine positive drug (PRX), Saline and CNO group. In Saline and CNO group, chemical genetic virus was used to inhibit the hippocampal astrocytes. Except for control group, the other groups were subjected to SPS modeling. After 7 days, the EA, Saline and CNO group were treated with EA at Baihui and Zusanli, while PRX group was given paroxetine solution for 10 days. Fear conditioning test and elevated plus maze test were used to evaluate fear memory extinction and anxiety-like behaviors, and the CNO group was administered CNO 30 minutes before the tests start. Immunofluorescence staining was used to observe the changes in the number and morphology of hippocampal astrocytes, and hippocampal expressions of GFAP and CX43 proteins were detected using Western blotting. RESULTS: In the mouse models with SPS, EA intervention significantly reduced the freezing time during fear re-exposure for 3-15 min and in the fear extinction phase. EA intervention also significantly increased the extinction coefficient, time spent in the open arms, the mean fluorescence intensity of GFAP, the number of astrocyte branches 50 μm from the soma, and the expression of CX43 proteins in the hippocampus of SPS mice. CONCLUSIONS: EA at Baihui and Zusanli improves fear memory extinction and anxiety-like behaviors in SPS mice by activating hippocampal astrocytes.
[ Decoction alleviates depression-like behaviors in rats exposed to chronic unpredictable mild stress by modulating tryptophan metabolism and the BDNF signaling pathway].
Meng T, Qin M, Xia Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045039 · Full text
OBJECTIVES: To evaluate the regulatory effects of Decoction on tryptophan metabolism, inflammation, and neurotrophic factor-related signaling pathways and its potential antidepressant effects in a rat model of depressio...
OBJECTIVES: To evaluate the regulatory effects of Decoction on tryptophan metabolism, inflammation, and neurotrophic factor-related signaling pathways and its potential antidepressant effects in a rat model of depression induced by chronic unpredictable mild stress (CUMS). METHODS: Adult male SD rat models of CUMS-induced depression were randomized into CUMS model group, fluoxetine group, low-dose Decoction group (LZZCD), and high-dose Decoction group (HZZCD) (=10), with another 10 normal rats as the control group. After modeling, the rats received daily drug interventions via gavage for 4 weeks. Forced swimming test, tail suspension test, and voluntary activity recording were used to assess depressive-like behaviors of the rats. HE staining, Western blotting and ELISA were used to evaluate the changes in brain tissue pathologies, tryptophan metabolism, neurotransmitter levels, inflammation and brain-derived neurotrophic factor (BDNF)-related pathways of the rats. RESULTS: The rat models with CUMS showed significantly increased immobility and reduced swimming and struggling time. Both fluoxetine and Decoction at the two doses markedly alleviated depressive-like behaviors of the rat models, and high-dose Decoction produced the strongest ameliorating effect. Decoction treatment reduced brain injury scores of the rats, upregulated TPH2 and downregulated IDO, KMO, and MAO-A expressions in the hippocampus, causing also inhibition of the NF‑κB/NLRP3 pathway and increased hippocampal expressions of TrkB, p-CREB, p-AKT, and p-ERK. ELISA results demonstrated that Decoction treatment increased Trp, 5-HT, and 5-HIAA levels, decreased the levels of Kyn and inflammatory cytokines, and upregulated BDNF expression in the hippocampus of the rat models. CONCLUSIONS: Decoction alleviates depressive-like behaviors and brain pathologies in CUMS rats by regulating tryptophan metabolism, enhancing synthesis and reducing degradation of neurotransmitters, inhibiting inflammatory response, and upregulating the BDNF signaling pathway.
[Modified Decoction improves cognitive function of TX mice with Wilson's disease by inhibiting the PKR/eIF2α pathway].
Xu C, Han Y, Cheng N … +1 more , Dong J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045038 · Full text
OBJECTIVES: To assess the effect of the Modified Decoction (MGDD, developed based on the strategy in traditional Chinese medicine) for improving cognitive function in a PKR-silenced Wilson's disease (WD) TX mouse model...
OBJECTIVES: To assess the effect of the Modified Decoction (MGDD, developed based on the strategy in traditional Chinese medicine) for improving cognitive function in a PKR-silenced Wilson's disease (WD) TX mouse model and explore the underlying mechanism. METHODS: Thirty-six TX mice were randomized into TX group, TX+MGDD group, C16 group, and C16+MGDD group. In C16 and C16+MGDD group, the mice received daily intraperitoneal injections of 300 μg/kg C16 (a PKR inhibitor) for 30 days, and saline injections were given in the other two groups; after WD modeling, the mice in TX+MGDD and C16+MGDD groups received MGDD gavage for 4 weeks, while the other two groups were given saline gavage. After the treatments, the mice were examined using behavioral tests, followed by immunofluorescence staining, TUNEL staining, TEM, RT-qPCR and Western blotting analysis of the brain tissue. RESULTS: In behavioral tests, the mice in C16+MGDD group showed significantly shorter time spent in the perimeter than those in C16 group without significant differences in other parameters. Immunofluorescence staining revealed obviously lowered hippocampal oxidative stress level in C16, TX+MGDD, and C16+MGDD groups compared with TX group. Both MGDD and C16 treatment alone increased the number of hippocampal synapses and vesicles and improved ultrastructural synaptic damages, but their combination exhibited no synergistic effect. The C16+MGDD group showed significantly higher expressions of PSD93, PSD95, synapsin1 and synaptophysin than C16 group, but had comparable PSD93 expression with TX+MGDD group. While the mRNA expressions in the PKR/eIF2α pathway were similar between C16+MGDD and C16 groups, the protein levels of P-eIF2α and CHOP were significantly lower and P-CREB protein level was higher in C16+MGDD group. CONCLUSIONS: MGDD improves cognitive dysfunction in WD TX mice possibly by inhibiting the PKR/eIF2α pathway, promoting expressions of synaptic proteins, and improving synaptic structure and function.
[Overexpression of miR-593-5p inhibits migration, invasion and proliferation and promotes apoptosis of gastric cancer cells by targeting PLK1].
Dong B, Peng J, Li J … +2 more , Meng Y, Yang X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045037 · Full text
OBJECTIVES: To explore the role of miR-593-5p targeting Polo-like kinase 1 (PLK1) in regulating biological behaviors of human gastric cancer (GC) cells. METHODS: Four GC cell lines (MGC-803, AGS, HGC-27, and MKN-45) and...
OBJECTIVES: To explore the role of miR-593-5p targeting Polo-like kinase 1 (PLK1) in regulating biological behaviors of human gastric cancer (GC) cells. METHODS: Four GC cell lines (MGC-803, AGS, HGC-27, and MKN-45) and normal human gastric mucosal epithelial GES-1 cells were examined for miR-593-5p and PLK1 expressions using RT-PCR, and MGC-803 cells with the lowest miR-593-5p expression and MKN-45 with highest miR-593-5p expression were selected for subsequent experiments. TargetScan7.2 was used to predict the binding between miR-593-5p and PLK1. MGC-803 cells were transfected with miR-593-5p mimic or mimic NC via liposome, and MKN-45 cells were transfected with miR-593-5p inhibitor or inhibitor NC. The changes in cellular PLK1 protein expression levels were detected using Western blotting, and the changes in biological behaviors of the cells were evaluated using scratch assay, Transwell assay, CCK-8 assay, and flow cytometry. RESULTS: Compared with GES-1 cells, the GC cell lines showed significantly downregulated miR-593-5p and upregulated PLK1 expressions. TargetScan7.2 identified binding sites between miR-593-5p and PLK1 3'UTR. In MGC-803 cells, miR-593-5p overexpression caused significant reduction of PLK1 protein expression, inhibited cell migration, invasion, and proliferation, and promoted cell apoptosis. Conversely, miR-593-5p inhibition in MKN-45 cells upregulated PLK1 expression, enhanced cell migration, invasion, and proliferation, reduced cell apoptosis. CONCLUSIONS: miR-593-5p overexpression inhibits GC cell migration, invasion, and proliferation, and promotes apoptosis, likely by directly downregulating PLK1, suggesting the role of miR-593-5p as a tumor suppressor in GC and its potential therapeutic relevance.
[ Capsule alleviates glucocorticoid-induced osteoporosis in rats by inhibiting vascular endothelial cell senescence and promoting bone formation].
Deng Z, Wang Z, Meng S … +4 more , Yang Y, Yang Y, Fan L, Wang L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045036 · Full text
OBJECTIVES: To investigate the role of cellular senescence in glucocorticoid-induced osteoporosis and explore the therapeutic mechanism of (JTG) Capsule. METHODS: Cultured human umbilical vein endothelial cells (HUVECs)...
OBJECTIVES: To investigate the role of cellular senescence in glucocorticoid-induced osteoporosis and explore the therapeutic mechanism of (JTG) Capsule. METHODS: Cultured human umbilical vein endothelial cells (HUVECs) and mouse pre-osteoblasts (MC3T3) were treated with methylprednisolone (MPS) or MPS combined with JTG Capsule dissolved in saline. HUVEC senescence pathways and repair capacity were analyzed using Western blotting, SA-β-Gal staining, DCFH-DA assay, scratch wound healing, and RT-PCR. The osteogenic potential of MC3T3 cells was assessed using immunofluorescence staining, ALP staining, Alizarin Red S staining, and RT-PCR. Osteoclast differentiation was evaluated by TRAP staining. Thirty 3-week-old female SD rats were randomized into control, MPS, and MPS+JTG groups, and the rats in the latter two groups received daily intraperitoneal MPS injections and treated with gavage of saline or JTG Capsule suspension for 3 months. Femurs and venous blood were collected from the rats for micro-CT analysis of femoral bone volume fraction and detection of serum bone metabolism markers. RESULTS: Network pharmacology revealed that the active components of tiger bone had numerous intersection targets with glucocorticoid-induced osteoporosis with a strong binding affinity to cellular senescence-related targets such as P53. In MPS-treated HUVEC-derived osteoclasts, treatment with JTG Capsule significantly inhibited the expressions of P53 and P21, attenuated oxidative stress, and enhanced cell migration and angiogenic capacity. Similarly, JTG Capsule significantly enhanced osteogenic and mineralization capacities of MC3T3 cells and suppressed osteoclast differentiation. In the rat models, intraperitoneal MPS injection for 14 days resulted in significant bone loss in the femur, and JTG Capsule treatment obviously alleviated bone loss and ameliorated the disorder in serum bone metabolic markers. CONCLUSIONS: JTG Capsule alleviates MPS-induced HUVEC senescence, enhances osteogenic capacity and suppresses osteoclastogenesis in MC3T3 cells, and promotes intraosseous angiogenesis to improve glucocorticoid-induced osteogenesis inrats.
[Hollow copper sulfide nanocomposites combined with photothermal and photodynamic therapy inhibits malignant behaviors of esophageal cancer cells].
Yang P, Ji A, Liao S … +6 more , Yao H, Gao Z, Chen P, Cheng H, Gao S, Shi L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045035 · Full text
OBJECTIVES: To develop a hollow CuS-based nanoparticles loaded with the photosensitizer IR780, investigate its photothermal and photodynamic (PTT-PDT) effects against esophageal cancer cells and analyze the underlying me...
OBJECTIVES: To develop a hollow CuS-based nanoparticles loaded with the photosensitizer IR780, investigate its photothermal and photodynamic (PTT-PDT) effects against esophageal cancer cells and analyze the underlying mechanisms. METHODS: Hollow CuS nanoparticles were synthesized using a sacrificial-template strategy, and IR780 was encapsulated within a lauric acid matrix to serve as a phase-change material for preparing IR780@CuS composite nanoparticles. The composite nanoparticles were characterized for morphology and structural attributes using transmission electron microscopy, X-ray diffraction, and UV-visible spectroscopy. The effects of IR780@CuS on proliferation, invasion, and migration of esophageal cancer cells under near-infrared (NIR) irradiation (808 nm, 1.5 W/cm², 5 min) were assessed using CCK-8 assay, live/dead staining, reactive oxygen species, mitochondrial membrane potential assay, wound-healing assay, and Transwell assay. The PTT-PDT therapeutic efficacy and biosafety of IR780@CuS was evaluated in a mouse model bearing subcutaneous esophageal cancer xenografts. RESULTS: The synthesized IR780@CuS nanoparticles exhibited a uniform quasi-spherical morphology with a photothermal conversion efficiency of 44.0%. Under NIR irradiation, IR780@CuS produced pronounced synergistic PTT-PDT effects against KYSE150 cells, causing a significant reduction of cell viability and marked suppression of cell proliferation, migration, and invasion. In the tumor-bearing mice, IR780@CuS and 808 nm laser irradiation exhibited strong synergistic PTT-PDT effects and significantly inhibited tumor growth with a good biocompatibility. CONCLUSIONS: The IR780@CuS composite nanoparticles achieve synergistic PTT-PDT antitumor activity in esophageal cancer cells which can be a promising strategy for combined therapy and targeted drug delivery for esophageal cancer.
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