Current Molecular Medicine[JOURNAL]
Sun
200 papers
miR-144/451: A Regulatory Role in Inflammation.
Zhu J, Feng Y, Zhang L … +3 more , Pang X, He S, Fang L
Curr Mol Med · 2025 · PMID 39506440 · Publisher ↗
BACKGROUND: Inflammation is the natural defense mechanism of the body in response to injury, infection, or other stimuli. Excessive or persistent inflammatory responses can lead to the development of inflammatory disease...
BACKGROUND: Inflammation is the natural defense mechanism of the body in response to injury, infection, or other stimuli. Excessive or persistent inflammatory responses can lead to the development of inflammatory diseases. Therefore, elucidating the regulatory mechanisms of inflammatory cells is crucial for understanding the pathogenesis of such diseases and devising novel therapeutic approaches. Moreover, miR-144/451 plays an important role in erythroid maturity and tumour development. Herein, we have reviewed the regulatory role of miR-144/451 in inflammation. METHODS: Papers on miR-144, miR-451, and inflammation were retrieved from PubMed and Web of Science to be analysed and summarised. RESULTS: miR-144/451 plays a significant role in modulating inflammatory responses. Pro- and anti-inflammatory gene transcription is regulated by miR-144/451 binding to the 3' untranslated regions. Studies have shown that miR-451 inhibits the activation of various inflammatory cells, including macrophages, neutrophils, and T lymphocytes, thereby reducing the release of inflammatory mediators. However, miR-144 expression varies in different inflammatory diseases. miR-144 expression is downregulated in macrophages after induction by lipopolysaccharide, cysteine, or Mycobacterium tuberculosis, which promotes the secretion of inflammatory mediators; nonetheless, miR-144-3p overexpression in macrophages can aggravate atherosclerosis. Meanwhile, miR-144 overexpression prevents disruption of the lung endothelial cell barrier, whereas it exacerbates endothelial cell injury in Crohn's disease. CONCLUSION: miR-144/451 may serve as a potential target for the treatment of inflammatory diseases.
NEDD4 Knockdown Suppresses Human Endometrial Stromal Cell Growth and Invasion by Regulating PTGS2-Mediated Ferroptosis in Endometriosis.
Lao J, Hu P, Wan Y … +3 more , Shu M, Chen J, Yang H
Curr Mol Med · 2025 · PMID 39501947 · Publisher ↗
BACKGROUND: Endometriosis (EM) is a gynecological disease characterized by the benign growth of endometrial tissue outside the uterus. Upregulation of neuronally expressed developmentally downregulated 4 (NEDD4) has been...
BACKGROUND: Endometriosis (EM) is a gynecological disease characterized by the benign growth of endometrial tissue outside the uterus. Upregulation of neuronally expressed developmentally downregulated 4 (NEDD4) has been reported to accelerate endometrial cancer progression. OBJECTIVES: We explored whether abnormal expression of NEDD4 is correlated with EM. METHODS: Endometrial tissue in patients without endometriosis was used to develop the original generation of endometrial stromal cells (ESCs). Different types of endometrial tissue of patients with endometriosis were used to measure the expression of NEDD4 by immunohistochemistry (IHC) and western blotting. Its biological functions in ESCs were investigated using a cell counting kit-8 assay, fluorescein diacetate (FDA) staining, and Transwell invasion assays. Additionally, its involvement in ferroptosis was assessed by measuring Fe2+, malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) levels and the expression of ferroptosis markers. RESULTS: Compared with normal controls, NEDD4 levels were significantly elevated in the endometrial tissue of patients with EM. Furthermore, NEDD4 expression was higher in the ectopic endometrium than in the eutopic endometrium. NEDD4 knockdown reduced the viability and invasive capacity of ESCs, increased Fe2+, MDA, and ROS levels, and decreased GSH content. Further analysis revealed that NEDD4 knockdown promoted ferroptosis in ESCs by increasing the expression of prostaglandin-endoperoxide synthase 2 (PTGS2). As an E3 ubiquitin ligase, NEDD4 reduced PTGS2 protein levels by accelerating its ubiquitination and subsequent proteasomal degradation. CONCLUSION: These findings suggest that inhibiting NEDD4 reduces ESC growth and invasion in EM by regulating PTGS2-dependent ferroptosis.
Emerging Applications of Medical Nanorobots in Health Care: Current Trends and Future Prospects.
Swain SK, Sahu PK, Jena BR … +1 more , Acharya B
Curr Mol Med · 2025 · PMID 39501946 · Publisher ↗
Medical nanorobots and nanobots are at the forefront of therapy and diagnostics, potentially improving human health by enabling previously inaccessible treatments. This review explores critical issues concerning the desi...
Medical nanorobots and nanobots are at the forefront of therapy and diagnostics, potentially improving human health by enabling previously inaccessible treatments. This review explores critical issues concerning the design, components, signaling, structure, and roles of nanorobots and nanobots while elucidating the distinctions between microrobots and nanorobots or microrobotics and nanorobotics as well. By complementing traditional medical procedures, nanorobotic technology offers a rapid, safe, and potentially beneficial pathway toward early clinical applications. It finds numerous applications in both current and future pharmacological and medical advancements. The current and future applications of various nanorobots, such as DNA origami nanorobots, nucleic acid robots, microbivore nanorobots, respirocyte nanorobots, and orthodontic nanorobots, are briefly discussed. In the future, nanobots will likely be prominently featured in hospitals and pharmacies for individuals or specialized groups with specific needs. Continuous innovation and improvement of these technologies, addressing these technical challenges, will broadly advance research in micro/nanorobotics for medical diagnosis and treatment.
Combination Antitumor Activation of Anlotinib with Radiofrequency Ablation in Human Medullary Thyroid Carcinoma.
Zhao Z, Ma X, Li Y … +4 more , Zhou SH, Zang LE, Feng F, Li N
Curr Mol Med · 2025 · PMID 39473258 · Publisher ↗
INTRODUCTION: Currently, Medullary Thyroid Carcinoma (MTC) is considered a kind of rare neuroendocrine tumor, and molecular-targeted drugs have previously been used for MTC treatment. However, the prognosis of MTC patien...
INTRODUCTION: Currently, Medullary Thyroid Carcinoma (MTC) is considered a kind of rare neuroendocrine tumor, and molecular-targeted drugs have previously been used for MTC treatment. However, the prognosis of MTC patients is still unsatisfactory. In the present work, we aimed to explore the antitumor activity of the molecularly targeted drug anlotinib in combination with radiofrequency ablation on MTC. METHODS: 44 MTC clinical specimens were involved. The targets of anlotinib in malignant cells were examined by qPCR. We cultured MTC cells line TT and treated with a series of concentration of TKIs. Then measure the inhibitory rates of TT cell survival. We established a subcutaneous tumorigenic model in nude mice to examine the antitumor effects of anlotinib combined with different RFA conditions. RESULTS: The targets of anlotinib were clearly expressed in MTC tissue specimens, and the expression level of these factors was much higher in MTC clinical specimens than in nontumor tissues. At the same time, anlotinib or Radiofrequency Ablation (RFA) showed clear antitumor activity against the MTC cell line TT (TT cells) and the tumor tissue it formed. CONCLUSION: These results indicated that the combination of anlotinib with RFA could be a promising therapeutic strategy for MTC treatment.
Associations between Gut Microbiota and Microbial Metabolites in Adjuvant-induced Arthritis Rats with Moist Heat Arthralgia Spasm Syndrome.
Sun Y, Gong C, Pan L … +3 more , Jiang H, Chen W, Wang Y
Curr Mol Med · 2025 · PMID 39473257 · Publisher ↗
BACKGROUND: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. According to traditional chinese medicine (TCM) syndromes theory, moist heat arthralgia spasm syndrome is the most prevalent syndrome of RA...
BACKGROUND: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. According to traditional chinese medicine (TCM) syndromes theory, moist heat arthralgia spasm syndrome is the most prevalent syndrome of RA patients in the active period. However, the mechanism of alteration of gut microbiota in RA with moist heat arthralgia spasm syndrome has not been reported until now. OBJECTIVE: This study focused on the alteration of gut microbiota in adjuvant-induced arthritis (AA) rats with moist heat arthralgia spasm syndrome, elaborated its regulation mechanism, and analyzed the associations between gut microbiota and microbial metabolites. METHODS: The disease-syndrome combination rat model of RA with moist heat arthralgia spasm syndrome was constructed with AA under damp-heat stimulating. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum biochemical indicators. Damages of ankle joints were observed using hematoxylin and eosin (H&E). 16 small ribosomal subunit RNA (16S rRNA) gene sequencing was conducted to assess the gut microbiota composition and function on feces from rats. Alterations in fecal metabolites profiling were evaluated by fecal metabolomics through liquid chromatography-mass spectrometry (LC-MS) and gas chromatography-mass spectrometry (GC-MS). Pearson correlation analysis was performed to explore the associations of altered gut microbiota and microbial metabolites in Model rats. RESULTS: The imbalance of gut microbiota in Model rats was accompanied by metabolic disorders. Lactobacillus, Prevotellaceae_NK3B31_group, Allobaculum, Prevotellaceae_UCG_001, Alloprevotella, and Dubosiella were found to be dominant genera in Model rats. In total, 357 metabolites were significantly altered in Model rats and predominantly enriched into fatty acid degradation and glycerophospholipid metabolism. Pearson correlation analysis showed that TNF-α and IL-1β were associated with Prevotellaceae_Ga6A1_group and 3R-hydroxy-docosan-5S-olide, alpha-N-(3-hydroxy-14-methyl-pentadecanoyl)-ornithine, 17-methyl-trans-4,5- methylenenona-decanoic acid, Semiplenamide F. CONCLUSION: The key differential microbiota genera and differential microbial metabolites may become important targets for the treatment of RA and provide the theoretical basis for exploring the pathogenesis of RA.
Cancer-associated Fibroblasts (CAFs) Regulate Lung Cancer Malignant Progression by Transferring SERPINE2 (PN1) via Exosomes.
Chen Y, Zhu S, Yang L … +2 more , Lu Y, Ye X
Curr Mol Med · 2025 · PMID 39473098 · Publisher ↗
BACKGROUND AND AIM: Cancer-associated fibroblasts (CAFs), one of the most abundant stromal cell types in the tumor microenvironment (TME), are potential targets for cancer treatments such as lung cancer. However, the und...
BACKGROUND AND AIM: Cancer-associated fibroblasts (CAFs), one of the most abundant stromal cell types in the tumor microenvironment (TME), are potential targets for cancer treatments such as lung cancer. However, the underlying mechanism by which CAFs promote lung cancer progression remains elusive. METHODS: We obtained primary CAFs, normal fibroblasts (NFs), and their exosomes and constructed protease nexin-1 (PN1) stably silenced or over-expressed CAFs cells using lentivirus. Bioinformatics was used to obtain the expression of PN1 in lung cancer and normal tissues, the relationship with overall survival, and the enriched pathways. The MTT and Transwell assays were performed to detect the proliferation, migration, and invasion abilities of lung cancer cells after treatment. Western blotting, qRT-PCR, immunohistochemistry, and xenograft models were used to illustrate the role of CAFs in lung cancer progression via exosomes. RESULTS: CAFs-derived exosomes, in which PN1 was more highly expressed than that in NFs-derived ones, effectively promoted the proliferation, migration, and invasion potentials of lung cancer cells A549 and H1975. Meanwhile, the PN1 expression was higher in lung cancer tissues than that in normal tissues and was negatively associated with the overall survival rate of lung cancer patients. More importantly, over-expressing or silencing of PN1 in A549 and H1975 cells promoted or inhibited cell proliferation, migration, and invasion, correspondingly. Furthermore, treated with PN1 overexpressing CAFs-derived exosomes, the lung cancer cells proliferation, migration, and invasion varied positively and were accompanied by activation of Toll-like and NF- κB signaling pathways. However, this phenomenon can be reversed by AN-3485, an antagonist of the Toll-like pathway. Finally, overexpression of PN1 leads to accelerated tumor growth by increasing the expression of the proliferation biomarker Ki67 and activation of the NF-κB signaling pathway in vivo. CONCLUSION: CAFs promoted lung cancer progression by transferring PN1 and activating the Toll-like/NF-κB signaling pathway via exosomes.
M2-like Macrophages-derived CCL17 Promotes Esophageal Squamous Cell Carcinoma Metastasis and Stemness via Activating CCR4-mediated ERK/PD-L1 Pathway.
Jin C, Lu L, Gao J … +1 more , Chen L
Curr Mol Med · 2025 · PMID 39473097 · Full text
BACKGROUND AND OBJECTIVE: High morbidity, high mortality and poor prognosis of esophageal squamous cell carcinoma (ESCC) highlights the urgent need for novel therapeutic strategies against ESCC. The current study address...
BACKGROUND AND OBJECTIVE: High morbidity, high mortality and poor prognosis of esophageal squamous cell carcinoma (ESCC) highlights the urgent need for novel therapeutic strategies against ESCC. The current study addresses the precise role of M2-like macrophages-derived CCL17 in ESCC progression and to thoroughly elucidate the intrinsic molecular mechanisms. METHODS: In this work, for functional experiments, Eca109 cells cultivated in M2-CM were treated with anti-IgG (50 μg/ml) or anti-CCL17 (50 μg/ml) to expound the tumorpromoting effects of M2-like macrophage-derived CCL17 in ESCC. Moreover, for rescue experiments, Eca109 cells were treated with CCL17 (50 ng/ml) and/or CCR4 antagonist AZD2098 (20 μM) to probe whether CCL17 could influence the malignant behaviors including migration, invasion and stemness of ESCC cells via activating CCR4/ERK/PD-L1 pathway. RESULTS: Markedly enhanced CCL17 secretion was observed in M2-like macrophages. CCL17 bound to CCR4 to activate ERK/PD-L1 signaling. M2-like macrophagesderived CCL17 facilitated ESCC cell migration and invasion and enhanced stemness characteristics of ESCC cells, which were partially reserved by AZD2098 treatment. The tumor-promoting effects of M2-like macrophages-derived CCL17 on ECSS was depended on the activation of CCR4/ERK/PD-L1 pathway. CONCLUSION: To conclude, M2-like macrophages-derived CCL17 could facilitate ESCC cell migration and invasion and enhance stemness characteristics of ESCC cells via activating CCR4/ERK/PD-L1 signaling.
Advances in the Study of the Pathogenesis of Vogt-Koyanagi- Harada Syndrome.
Wang MN, Zhang L, Zhou HY … +5 more , Zhong W, Zhang H, Bi MM, Wang L, Lu J
Curr Mol Med · 2025 · PMID 39449345 · Full text
Vogt-Koyanagi-Harada syndrome (VKHS) is a common type of uveitis characterized by the invasion of melanocyte-rich tissues. In recent years, the incidence of VKHS has been increasing yearly, and its specific pathogenesis...
Vogt-Koyanagi-Harada syndrome (VKHS) is a common type of uveitis characterized by the invasion of melanocyte-rich tissues. In recent years, the incidence of VKHS has been increasing yearly, and its specific pathogenesis has not yet been elucidated. However, its pathogenesis has been a hot topic of research. The clinical course of VKHS is characterized by the early involvement of the posterior segment of the eye, including exudative retinal detachment, optic papillitis, bilateral diffuse chorioretinitis, etc. If treated improperly or with delayed treatment, the inflammation may gradually spread to the anterior segment of the eye, leading to vision loss or even vision. This study examines the pathogenesis of VKHS. It reviews the progress of research on the pathogenesis of VKHS, which will help to improve the understanding of VKHS and provide a reference for subsequent studies.
Evolutionary Sequences and Structural Information-driven Reconstruction of New Insulin-like Growth Factor-I Peptide Variants.
Khan N, Althobiti M, Chinnadurai RK … +2 more , Alharbi S, Kumar R
Curr Mol Med · 2025 · PMID 39428935 · Publisher ↗
BACKGROUND: Insulin-like growth factor-I (IGF-I) is crucial in controlling cell growth, proliferation, and apoptosis. Its strong link to the development of cancers such as breast, prostate, lung, thyroid, and colorectal...
BACKGROUND: Insulin-like growth factor-I (IGF-I) is crucial in controlling cell growth, proliferation, and apoptosis. Its strong link to the development of cancers such as breast, prostate, lung, thyroid, and colorectal has positioned the IGF-1 signalling pathway as a promising target for novel cancer therapies. When activated, the IGF-1 receptor (IGF-1R) binds to IGF-I, playing a central role in promoting tumour cell growth and survival. METHODS: In this study, we combined evolutionary sequences with structural and functional data of IGF-1 to reconstruct ancestral sequences and design novel IGF-1 peptide variants. RESULTS: The insulin-like growth factor system exhibits a vast sequence diversity, yet it shares a similar structural topology with conserved three pairs of disulfide linkages. Our study reveals that IGF-1 is associated with the IGF system of cell surface receptors through protein-protein interactions. Reconstructed IGF-1 variants show similar structure fold to reported viral IGF-1 competitive antagonists. CONCLUSION: This new insight guides the design of novel natural IGF-1 mimic peptides. It enhances our understanding of IGF-1's functionality and opens new avenues for the development of therapeutic peptides and small molecules as anticancer agents.
Exploring the Dual Role of MALAT1 in Thyroid Tumorigenesis: Oncogenic or Tumor Suppressor?
Anbiyaee O, Ghaedrahmati F, Salehi AM … +4 more , Khodadadi A, Kempisty B, Farzaneh M, Dari MAG
Curr Mol Med · 2025 · PMID 39421983 · Publisher ↗
Thyroid cancer is the most prevalent form of endocrine cancer. Therefore, the administration of new therapeutic agents for thyroid cancer patients is necessary. One of the recent successes in thyroid cancer research is t...
Thyroid cancer is the most prevalent form of endocrine cancer. Therefore, the administration of new therapeutic agents for thyroid cancer patients is necessary. One of the recent successes in thyroid cancer research is the identification of the role of signaling pathways in the pathogenesis of the disease. Emerging evidence reveals that long non-coding RNAs (lncRNAs) can serve as novel therapeutic approaches for the diagnosis and treatment of thyroid cancer. The lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) plays key roles in gene expression, RNA processing, and epigenetic regulation. It is believed that MALAT1 can regulate several cancer-related processes, including tumour cell growth, proliferation, and metastasis. MALAT1 is involved in the pathogenesis of thzroid cancers by targeting multiple downstream targets and miRNA/mRNA axes. Here, we summarize the emerging roles of MALAT1 in this cancer.
CircRNA in Digestive Diseases: Recent Advances in Fundamental Mechanism and Clinical Potential.
Ji Y, Zhang S, Cai T … +3 more , Fu L, Deng Q, Zhu P
Curr Mol Med · 2025 · PMID 39421982 · Publisher ↗
Circular RNAs (circRNAs), a class of non-coding RNAs characterized by their closed-loop structure, are widely present in the body and exhibit greater stability compared to conventional linear RNAs. With the development o...
Circular RNAs (circRNAs), a class of non-coding RNAs characterized by their closed-loop structure, are widely present in the body and exhibit greater stability compared to conventional linear RNAs. With the development of molecular biology, circRNAs are gradually considered as a prognostic indicator and therapeutic target for various diseases. Research on the mechanism of circRNA in various diseases has become an important direction. In addition, digestive diseases are becoming more common as people's eating habits change, and the incidence and mortality of severe digestive system tumors are increasing year by year. The study of circRNA in digestive diseases provides us with a new way to improve the diagnosis and treatment of digestive diseases. This article provides a comprehensive review of the research literature on circRNAs in digestive system diseases over the past five years (2019- 2023) and covers aspects such as circRNA functions and underlying mechanisms. CircRNA has been implicated in a variety of digestive diseases. In these diseases, circRNA primarily acts as a microRNA (miRNA) sponge, interacting with miRNA to regulate the expression levels of genes associated with signaling pathways, and there is abundant research on the effects of circRNAs on drug resistance, cell proliferation, invasion, apoptosis, and poor prognosis. This article aima to discuss the current status of research on circular RNA and its key areas in digestive system diseases. The review aims to provide valuable insights for further research on the role of circular RNA in digestive system diseases and a reference for subsequent research.
Preparation of Menthyl 3-amino-4-(2,4,5-trifluorophenyl) Butyrate and Investigation of its Hypoglycemic Activity.
Kuang X, Su M, Li H … +4 more , Sheng X, Cai H, Xie S, Liu Z
Curr Mol Med · 2024 · PMID 39420727 · Full text
BACKGROUND: 3-Amino-4-(2,4,5-trifluorophenyl) butyric acid has potential pharmacological effects in promoting insulin secretion. Menthol promotes drug transdermal absorption and hypoglycemic effects. OBJECTIVE: The objec...
BACKGROUND: 3-Amino-4-(2,4,5-trifluorophenyl) butyric acid has potential pharmacological effects in promoting insulin secretion. Menthol promotes drug transdermal absorption and hypoglycemic effects. OBJECTIVE: The objective of the study was to combine the 3-amino-4-(2,4,5- trifluorophenyl) butyric acid and menthol to develop a new candidate drug molecule that can be used as a hypoglycemic drug in type II diabetes. METHODS: In this study, the molecular structure of 3-amino-4-(2,4,5-trifluorophenyl) butyric acid in sitagliptin was modified by replacing pyrazine imidazole with menthol. The structure of the target compound was characterized by nuclear magnetic resonance (NMR). The anti-diabetic activity of BHF in N000180 BKS.Cg-Dock7m+/ +Leprdb/Nju mice with spontaneous diabetes was preliminarily studied. RESULTS: A potential multi-target drug molecule, 3-amino-4-(2,4,5-trifluorophenyl) butyrate (BHF), was synthesized by combining 3-amino-4-(2,4,5-trifluorophenyl) butyric acid and menthol. BHF is suitable for hyperglycemic mice and has a significant hypoglycemic effect; the low dose of 10 mg/kg-1 started to be effective, and the high dose of 40 mg/kg-1 was more effective than the positive drug metformin. CONCLUSION: In this study, BHF has been synthesized and presented significant antidiabetic activities.
Tumor Mutational Burden as a Biomarker of Immunotherapy Response: An Immunogram Approach in Onco-immunology.
Ansari A, Ray SK, Sharma M … +2 more , Rawal R, Singh P
Curr Mol Med · 2024 · PMID 39420726 · Publisher ↗
Immune checkpoint inhibitors have revolutionized cancer treatment by allowing T cells to reactivate. Tumor mutational burden (TMB) is a biomarker that has emerged as a viable diagnostic for locating patients who would be...
Immune checkpoint inhibitors have revolutionized cancer treatment by allowing T cells to reactivate. Tumor mutational burden (TMB) is a biomarker that has emerged as a viable diagnostic for locating patients who would benefit from immunotherapy in particular cancer types. Greater neo-antigens mean more opportunities for T cell identification, and TMB is clinically linked to better immune checkpoint inhibitors. Tumor foreignness is a cancer immunogram, and TMB can be used as a substitute for foreignness. The role of TMB analysis as an independent predictor of immunotherapy response in the context of immune checkpoint inhibitor medications is the subject of this mini-review.
Evaluation of the Safety and Efficacy of Curcumin-Synthesized Silver Nanoparticles in Rats Exposed to Chlorpyrifos During Puberty Development.
Rezaei M, Shakibaie M, Mohaqeq A … +5 more , Khoramroudi S, Mohaqiq Z, Aschner M, Samarghandian S, Farkhondeh T
Curr Mol Med · 2024 · PMID 39420715 · Publisher ↗
BACKGROUND: Silver nanoparticles (Ag-NPs) have garnered significant attention in recent years due to their therapeutic effects. Curcumin (CUR) has been utilized as a coating agent for synthesizing Ag-NPs, intended to act...
BACKGROUND: Silver nanoparticles (Ag-NPs) have garnered significant attention in recent years due to their therapeutic effects. Curcumin (CUR) has been utilized as a coating agent for synthesizing Ag-NPs, intended to act as a potential drug. OBJECTIVE: This study was designed to evaluate the safety and efficacy of curcuminsynthesized silver nanoparticles on rats exposed to chlorpyrifos (CPF) during their pubertal development. METHODS: Forty-two male Wistar rats, 23 days old, were selected and randomly divided into 7 groups (n=6) as follows: positive control, negative control, CPF (5 mg/kg), silver nanoparticles synthesized using curcumin at 40 μg/kg (CUR-Ag-NPs 40), CUR-Ag-NPs 80, CPF+ CUR-Ag-NPs 40, CPF+ CUR-AgNPs 80. All treatments were administered via gavage for 30 days. At the end of the study, rats were anesthetized using ketamine (50 mg/kg), and xylazine, (10 mg/kg) and blood was collected from the heart for serum analysis of liver enzymes, urea, and creatinine. RESULTS: Liver and kidney tissues were isolated for histopathological analysis. No significant differences were observed in serum levels of AST, ALT, and ALP enzymes as well as urea and creatinine levels among the different groups. Light microscopy observation revealed multifocal inflammatory mononuclear cell subsets in liver tissue associated with mild inflammatory mononuclear cell infiltration in the portal region in CPF, CUR-Ag-NPs 40, CUR-Ag-NPs 80, CPF+CUR-Ag-NPs 40, and CPF+CUR-Ag- NPs 80 groups. Histological examination of kidney tissue showed degenerative changes in the tubular epithelium, congestion, and mild infiltration of mononuclear inflammatory cells in the renal interstitial tissue in the CPF group, CUR-Ag-NPs 40, CUR-Ag-NPs 80, CPF+CUR-Ag-NPs 40 and CPF+CUR-Ag-NPs 80 groups. CONCLUSION: This study failed to establish the safety and efficacy of CUR-Ag-NP at 40 and 80 μg/kg in prepubertal rats exposed to CPF. However, further studies should be conducted to thoroughly characterize the efficacy of CUR-Ag-NP in developmental animal models.
The Apoptotic, Cytotoxic, and Anti-migration Effects of Sodium Deoxycholate in a Breast Cancer Cell Line and its Modulation on PON1 as a Predictive Risk Marker.
Tuluce Y, Alhammud H, Keles AY … +1 more , Kostekci S
Curr Mol Med · 2025 · PMID 39411938 · Publisher ↗
INTRODUCTION: Breast cancer is the most prevalent cancer among women and is usually treated with antineoplastic drugs. The present study examines the influence of sodium deoxycholate on the molecular pathways underlying...
INTRODUCTION: Breast cancer is the most prevalent cancer among women and is usually treated with antineoplastic drugs. The present study examines the influence of sodium deoxycholate on the molecular pathways underlying apoptosis, cytotoxicity, and the modulation of PON1 in the MCF-7 breast cancer cell line. Various doses were administered to test the hypothesis that it could potentially affect cancer cells. METHODS: The study examined the cytotoxic effect of sodium deoxycholate on MCF-7 cells and human mammary epithelial cells (CRL-4010) using the MTT method to detect its anticancer properties. Subsequently, the efficacy of the active dose on DNA fragmentation and apoptosis was examined using the apoptotic DNA ladder and Western blot methods. Additionally, oxidative stress index and cell migration tests were conducted. Notably, sodium deoxycholate did not cause DNA damage despite demonstrating cytotoxic effects on cells. RESULTS: The study found that sodium deoxycholate increased the levels of several pro-apoptotic proteins, leading to apoptosis. Moreover, it markedly diminishes the activity of paraoxonase and arylesterase of PON1, which are predictive risk markers for cancer. Furthermore, it was found to delay cell migration in a time-dependent manner. CONCLUSION: These findings suggest that sodium deoxycholate exhibits an antimetastatic effect in breast cancer cells, could be a valuable subject for further cancer research.
Potentiation of Tumor Hallmarks by the Loss of GULO, a Vitamin C Biosynthesis Gene in Humans.
Sekar G, Bahot A, Bansode M … +3 more , Phadnis A, Sarode SC, Sharma NK
Curr Mol Med · 2025 · PMID 39411937 · Publisher ↗
Vitamin C plays a significant role in various physiological functions. Humans depend on external sources of vitamin C due to the loss of the L-gulono-γ-lactone oxidase (GULO) gene that contributes to the synthesis of vit...
Vitamin C plays a significant role in various physiological functions. Humans depend on external sources of vitamin C due to the loss of the L-gulono-γ-lactone oxidase (GULO) gene that contributes to the synthesis of vitamin C. During the evolutionary loss of the GULO gene, physical, chemical, and biological factors were different from the present environmental settings. Besides the evolutionary genetic loss of the GULO gene, there is a gap in the insightful discussion on the potential implications of the non-functional GULO gene towards the predisposition of humans to cancer that faces hostile and carcinogenic environments. Various methods by which vitamin C modulates cellular processes related to cancer, including DNA repair, epigenetic changes, and redox balance, are discussed. Furthermore, we present experimental and clinical evidence indicating that vitamin C deficiency promotes tumor growth, metastasis, and therapy resistance, emphasizing its potential as a cancer phenotypic modulator. Therapeutic implications of restoring vitamin C levels in cancer treatment range from improving the efficacy of conventional medicines to exploiting metabolic vulnerabilities in tumors. The relevance of assessing vitamin C status in cancer patients and the basis for additional research into vitamin C supplementation as an adjuvant therapy is emphasized. This paper presents a comprehensive overview of the implications associated with the functional deficiency of the GULO gene in human subjects exhibiting diverse tumor hallmarks, encompassing ECM remodeling, hypoxia, epigenetic reprogramming, oxidative stress, and drug responsiveness.
Contribution of the Activated mTOR-STAT3 Pathway to the Pathogenesis of Focal Cortical Dysplasia Type IIIa in Pediatric Patients through Astrocyte Proliferation Mediation.
Wang J, Wu J, Li Y … +3 more , Lv Y, Zhang X, Kang L
Curr Mol Med · 2025 · PMID 39377376 · Publisher ↗
OBJECTIVE: The aim of this study was to detect the association between the mTOR-STAT3 pathway and focal cortical dysplasia type IIIa (FCD IIIa) in children. METHODS: A retrospective review was conducted based on 26 pedia...
OBJECTIVE: The aim of this study was to detect the association between the mTOR-STAT3 pathway and focal cortical dysplasia type IIIa (FCD IIIa) in children. METHODS: A retrospective review was conducted based on 26 pediatric patients diagnosed with FCD IIIa who underwent surgical intervention. These patients were selected from a cohort of 157 individuals presenting with temporal lobe epilepsy. For comparative analysis, a control group consisting of 5 children who underwent intracranial decompression was established. Immunohistochemistry, immunofluorescence, and western blot techniques were used to assess the expression levels of mTOR, P-mTOR, P-70s6k, STAT3, P-STAT3, and GFAP in brain tissue specimens obtained from the two groups. RESULTS: The mTOR-STAT3 pathway exhibited activation in the FCD IIIa group (all p < 0.01). Additionally, immunofluorescence analysis revealed that cells positive for PSTAT3 were identified as astrocytes. Moreover, within the FCD IIIa group, there was a marked elevation in the expression of the mTOR-STAT3 pathway in the hippocampus compared to the brain cortex tissue. CONCLUSION: The mTOR-STAT3 pathway was demonstrated to be substantially associated with FCD IIIa in pediatric patients. The activation of the mTOR-STAT3 signaling pathway may contribute to the pathogenesis of FCD IIIa in pediatric patients by modulating the proliferation of astrocytes.
Role of Nrf2 in Epilepsy Treatment.
Azadmanesh M, Farkhondeh T, Harifi-Mood MS … +3 more , Aschner M, Samini F, Samarghandian S
Curr Mol Med · 2025 · PMID 39350402 · Publisher ↗
Oxidative stress is a consequence of the disruption of the balance between the generation of reactive nitrogen and oxygen species and the biological system's ability to neutralize those reactive products. Oxidative stres...
Oxidative stress is a consequence of the disruption of the balance between the generation of reactive nitrogen and oxygen species and the biological system's ability to neutralize those reactive products. Oxidative stress is involved in the generation of many disorders, including epilepsy, which is a prevalent chronic neurological disease that affects the lives of millions of people around the world. Epilepsy is characterized by unforeseeable and repeated seizures that can be very disturbing. Studies have reported that oxidative stress occurs before and after seizures. A transcription factor named Nuclear factor erythroid-derived 2-related factor 2 (Nrf2) controls genes related to the induction of oxidative stress and defends cells against oxidative stress. The Nrf2 protein has seven different domains, ranging from Neh1 to Neh7. Each domain is responsible for a distinctive function of this protein. Keap1 binds to Nrf2, but during oxidative stress, Nrf2 detaches from the Keap1 protein, moves to the nucleus, and binds to DNA. The result of this translocation and binding is the initiation of transcription of detoxifying genes to control the harmful effects of oxidative stress. There is some evidence of oxidative stress involvement in epilepsy. In this review, we have listed potential Nrf2-related therapeutic targets for treating and controlling epilepsy, such as Berberis alkaloids, pentoxifylline, lovastatin, progesterone, and chrysin nanoparticles. These activators were tested in animals (in vivo) and cells (in vitro), and most of these experiments showed promising results in different epilepsy models. Finally, the results have suggested that the activation of Nrf2 can be an option for controlling epilepsy.
Exploring the Neuroprotective Potential of Icariin through Modulation of Neural Pathways in the Treatment of Neurological Diseases.
Sharma S, Mehan S, Khan Z … +5 more , Tiwari A, Kumar A, Gupta GD, Narula AS, Kalfin R
Curr Mol Med · 2025 · PMID 39328135 · Publisher ↗
Neuropathological diseases involve the death of neurons and the aggregation of proteins with altered properties in the brain. Proteins are used at the molecular level to categorize neurodegenerative disorders, emphasizin...
Neuropathological diseases involve the death of neurons and the aggregation of proteins with altered properties in the brain. Proteins are used at the molecular level to categorize neurodegenerative disorders, emphasizing the importance of protein-processing mechanisms in their development. Natural herbal phytoconstituents, such as icariin, have addressed these neurological complications. Icariin, the principal compound in Epimedium, has been studied for its antineuroinflammatory, anti-oxidative, and antiapoptotic properties. Recent scientific investigations have shown that icariin exhibits promising therapeutic and preventive properties for mental and neurodegenerative disorders. In preclinical, icariin has been shown to inhibit amyloid development and reduce the expression of APP and BACE-1. Previous preclinical studies have demonstrated that icariin can regulate proinflammatory responses in neurological conditions like Parkinson's disease, depression, cerebral ischemia, ALS, and multiple sclerosis. Studies have shown that icariin possesses neuroprotective properties by modulating signaling pathways and crossing the blood-brain barrier, suggesting its potential to address various neurocomplications. This review aims to establish a foundation for future clinical investigations by examining the existing literature on icariin and exploring its potential therapeutic implications in treating neurodegenerative disorders and neuropsychiatric conditions. Future research may address numerous concerns and yield captivating findings with far-reaching implications for various aspects of icariin.
Multiplex PCR System for the Diagnosis of Plague.
Wang W, Zhang X, Yu H … +1 more , Wang Z
Curr Mol Med · 2025 · PMID 39318207 · Full text
The plague caused by Yersinia pestis has a high case fatality rate. It is often transmitted from person to person through mosquito bites, causing serious disease transmission. Due to its clinical symptoms being very simi...
The plague caused by Yersinia pestis has a high case fatality rate. It is often transmitted from person to person through mosquito bites, causing serious disease transmission. Due to its clinical symptoms being very similar to influenza, it is difficult to detect by people. Traditional detection methods for Y. pestis mainly include bacterial culture and serological identification, which are cumbersome and require high experimental conditions. Therefore, a fast and effective detection method is very important. At present, polymerase chain reaction (PCR) is one of the methods for rapid detection of Y. pestis. In this review, we focus on the application, advantages, and disadvantages of multiplex PCR technology in clinical detection.
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