Journal of Molecular Histology最新文献

{"title":"Research progress on ferroptosis in head and neck squamous cell carcinoma","authors":"Yi Qiu,&nbsp;Yuyuan Su,&nbsp;Wenli Sai,&nbsp;Guijuan Feng","doi":"10.1007/s10735-025-10381-y","DOIUrl":"10.1007/s10735-025-10381-y","url":null,"abstract":"<div><p>Ferroptosis, a regulated iron-dependent cell death pathway driven by lipid peroxidation and mitochondrial dysfunction, has emerged as a critical player in diseases characterized by dysregulated iron metabolism and redox imbalance. In recent years, its therapeutic potential has garnered significant attention in head and neck squamous cell carcinoma (HNSCC), a malignancy notorious for its high incidence, frequent recurrence, and poor prognosis. This review systematically delineates the molecular underpinnings of ferroptosis in HNSCC pathogenesis and therapy, focusing on four interconnected axes: (1) iron homeostasis disruption, exemplified by dysregulation of the iron efflux channel ferroportin (FPN); (2) lipid peroxidation dynamics, mediated through key regulators such as SLC7A11; (3) mitochondrial remodeling, including structural and functional alterations during ferroptosis execution; and (4) critical signaling cascades, notably the PI3K-AKT-mTOR pathway, which orchestrates cellular survival and death decisions. Therapeutic exploration has identified ferroptosis inducers (e.g., erastin) as promising agents to disrupt redox equilibrium in HNSCC cells, while pharmacological inhibitors offer potential for mitigating off-target toxicity. Notably, combination strategies integrating ferroptosis modulation with conventional therapies or other programmed cell death mechanisms demonstrate synergistic efficacy, highlighting a paradigm shift in precision oncology. This study aims to provide a mechanistic framework for ferroptosis in HNSCC, bridging preclinical insights with translational opportunities. By elucidating context-dependent regulatory networks and optimizing therapeutic targeting, we propose novel strategies to overcome treatment resistance, ultimately improving clinical outcomes and quality of life for HNSCC patients. </p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143632498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ciliary neurotrophic factor (CNTF) contributes to pelvic organ prolapse by modulating collagen expression via the JAK2–STAT3 pathway","authors":"Zhonglei Xu,&nbsp;Qiyin Zhu,&nbsp;Ying Yang,&nbsp;Wenjun Shan,&nbsp;Fang Jiang,&nbsp;Qianli Zou,&nbsp;Wenyan Wang","doi":"10.1007/s10735-025-10383-w","DOIUrl":"10.1007/s10735-025-10383-w","url":null,"abstract":"<div><p>Pelvic organ prolapse (POP) is a prevalent condition that affects postmenopausal women and significantly impacts their quality of life. The most common potential causes include vaginal delivery, age, and obesity. However, the specific pathophysiological mechanisms involved remain unclear. Therefore, we conducted a comparative analysis of vaginal anterior wall-associated proteins between POP patients and non-POP patients using Masson staining, immunohistochemistry, western blotting, and real-time quantitative fluorescence PCR. Additionally, we investigated the effect of ciliary neurotrophic factor (CNTF) on collagen secretion by fibroblasts in cell culture and instantaneous transfection experiments. Furthermore, the role of CNTF in the development of POP was investigated by constructing a rat prolapse model in which bilateral ovaries were removed and vaginal delivery was simulated. The findings indicated that the anterior vaginal wall of POP patients exhibited high CNTF expression, low collagen I expression, and high collagen III expression. Furthermore, cell transfection experiments demonstrated that CNTF may inhibit collagen I expression and promote collagen III expression by activating the JAK2–STAT3 pathway. A rat model constructed by simulating vaginal delivery after bilateral ovary removal is also an appropriate animal model for studying POP.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined skin injury model from airblast overpressure and seawater immersion in rats: establishment, characterization, and mechanistic insights","authors":"Jinpeng Du,&nbsp;Zhao Li,&nbsp;Yi Kong,&nbsp;Wei Song,&nbsp;Zhongming Chen,&nbsp;Mengde Zhang,&nbsp;Yuyan Huang,&nbsp;Chao Zhang,&nbsp;Xu Guo,&nbsp;Linhao Hou,&nbsp;Yaxin Tan,&nbsp;Liting Liang,&nbsp;Yuzhen Wang,&nbsp;Yu Feng,&nbsp;Qinghua Liu,&nbsp;Jianjun Li,&nbsp;Dongzhen Zhu,&nbsp;Xiaobing Fu,&nbsp;Sha Huang","doi":"10.1007/s10735-025-10379-6","DOIUrl":"10.1007/s10735-025-10379-6","url":null,"abstract":"<div><p>In maritime operations, individuals often face the threat of combined injury caused by airblast overpressure and seawater immersion. Airblast overpressure, induced by explosions, leads to significant internal damage despite the absence of visible open wounds. Seawater immersion exacerbates injuries due to its high osmolarity, microbial content, and thermal conductivity. Given the critical role of the skin as the body’s largest organ, understanding its specific injuries in this scenario is imperative but currently underexplored. To bridge this gap, the study developed a novel rat skin combined injury model (RSCIM) in which rats were exposed to calibrated airblast overpressure followed by immediate seawater immersion. Physical simulations, histopathological examinations, and immunological assessments were used to confirm the model’s accuracy. Specifically, finite element analysis reveals that the epidermal layer could effectively disperse and resist the immediate effects of overpressure. Histologically, the epidermal layer after combined injury maintained a continuous and complete structure. The collagen fibers of dermis were dispersed and broken. There were scattered capillaries, red blood cells and no skin appendages within the adipose layer. The muscle layer was manifested by deformation and breakage of muscle fibers. The fluorescence intensity of iNOS tended to decrease as the distance from the explosion source increased, which demonstrated significant inflammatory effects in the skin with combined injury. Furthermore, the transcriptome sequencing data revealed major physiological changes caused by combined injury, including inflammatory response, ion transport, biomechanical response, apoptosis, etc. Notably, S100A9 serves as a critical marker for combined injuries in RSCIM, but its expression characteristics and localization during tissue injury still need to be further explored. The model provides a robust foundation for exploring the combined injury mechanisms of airblast overpressure and seawater immersion and developing targeted therapeutic approaches.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous mitochondria added on benefits for cellular prion protein overexpression in adipose-derived mesenchymal stem cells treatment on intracranial hemorrhage rat","authors":"Kun-Chen Lin,&nbsp;Jui-Ning Yeh,&nbsp;Pei‐Hsun Sung,&nbsp;Tsung-Cheng Yin,&nbsp;John Y. Chiang,&nbsp;Chi-Ruei Huang,&nbsp;Yi-Ling Chen,&nbsp;Yi-Ting Wang,&nbsp;Kuan-Hung Chen,&nbsp;Hon‐Kan Yip","doi":"10.1007/s10735-025-10382-x","DOIUrl":"10.1007/s10735-025-10382-x","url":null,"abstract":"<div><p>We examined whether combined exogenous mitochondria (Ex^Mito) and cellular prion protein overexpression (Ove-PrP^C) in adipose-derived mesenchymal stem cell (Ove-PrP^C in ADMSCs) therapy is superior to a single therapy for protecting the brain against intracranial hemorrhage (ICH) in rats. In vitro, compared with the control group, Ex^Mito transfusion into recipient cells (i.e., N2a cells) significantly increased under hypoxic conditions (<i>P</i> &lt; 0.001) and augmented ρ0 cell proliferation and cell-cycle activation (<i>P</i> &lt; 0.001). PrP^C−OE in ADMSCs exhibited higher resistance to H₂O₂-induced cell senescence and mitochondrial and DNA damage compared to ADMSCs (<i>P</i> &lt; 0.001). Rats were categorized into group 1 (sham-control), 2 (ICH), 3 [ICH + Ex^Mito (350 μg) by intracranial injection at 3 h after ICH], 4 [ICH + PrP^C−OE in ADMSCs (6.0 × 10⁵ cells) and intracranial injection and 1.2 × 10⁶ cells by intravenous injection)], and 5 (ICH + combined Ex^Mito + PrP^C−OE in ADMSCs). By day 28, the brain infarct volume, brain infarct area, inflammatory cell infiltration, and biomarkers for DNA and mitochondrial damage were highest in group 2, lowest in group 1, and significantly lower in group 5 than in groups 3 and 4. NeuN cells exhibited the opposite pattern for brain infarct volume, and neurological function (corner test) significantly improved in groups 3 and 4, with further improvement in group 5 compared with that in group 2 (<i>P</i> &lt; 0.0001). Combined Ex^Mito + PrP^C−OE ADMSCs therapy was superior to either therapy alone in mitigating the ICH-induced brain damage.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10382-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial transplantation via injection of exogenous mitochondria into blood reduces bleomycin-induced oxidative damages and mitochondrial dysfunction in lung tissue","authors":"Ahmad Salimi,&nbsp;Mohammad Shabani,&nbsp;Samira Pourmohammad Shahsavar,&nbsp;Aida Naserian,&nbsp;Saleh Khezri,&nbsp;Hamed Karroubian","doi":"10.1007/s10735-025-10386-7","DOIUrl":"10.1007/s10735-025-10386-7","url":null,"abstract":"<div><p>Mechanistic studies have been suggested that adverse effect of bleomycin is attributed to formation of free radicals, mitochondria damages, oxidative stress and inflammation in lung tissue. Mitochondria act as central regulators in the oxidative stress and inflammatory responses in lung tissue, then it can be a promising approach for management bleomycin-induced pneumotoxicity. In the current study, we aim to investigated the injection of exogenous mitochondria into blood as one of the most promising pharmacological approaches to reduce bleomycin-induced lung toxicity in rats. Rats were divided into 4 groups as control, bleomycin (5 mg/kg), bleomycin + mitochondria (250 µg/kg), and mitochondria (250 µg/kg) alone. After 2 weeks, the survival rate, weight changes of animals, wet/dry ratio of lung tissue, alterations of histopathology, hydroxyproline content, oxidative stress and mitochondrial biomarkers were determined. Except the survival rate, weight changes of animals and wet/dry ratio of lung tissue, administration of bleomycin resulted in significant alteration in GSH content, MDA level, hydroxyproline amount, collapse of mitochondrial membrane potential (MMP), reduction of succinate dehydrogenases (SDH) activity and histopathological abnormality in comparison with control group. While exogenous mitochondria could inhibit GSH depletion, reduce production of MDA, improve the activity of SDH, prevent loss of MMP and histopathological abnormality. To the best of our knowledge, our data provides the first direct experimental evidence that injection of exogenous mitochondria into blood is capable of ameliorating bleomycin-induced lung toxicity in rats. These findings support that mitochondrial transplantation can be a promising therapeutic strategy for bleomycin-associated mitochondrial dysfunction and lung damage.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective role of Tongxinluo in mitigating myocardial fibrosis in mice with acute myocardial infarction via neuregulin-1 upregulation and Inhibition of endothelium-interstitial transition","authors":"Zhen Li,&nbsp;Yu-jie Yin,&nbsp;Ya-ru Wei,&nbsp;Yi Liu,&nbsp;Ning-xin Han,&nbsp;Xiao-qi Wang,&nbsp;Yuan-jie Hao,&nbsp;Ya-fen Wang,&nbsp;Yun-long Hou,&nbsp;Zhen-hua Jia","doi":"10.1007/s10735-025-10378-7","DOIUrl":"10.1007/s10735-025-10378-7","url":null,"abstract":"<div><p>Acute myocardial infarction (AMI) is a leading cause of heart failure, often accompanied by myocardial fibrosis (MF), characterized by excessive extracellular matrix accumulation. Endothelial-to-mesenchymal transition (EndMT) plays a key role in MF progression post-AMI. Neuregulin-1 (NRG-1), a growth factor with cardioprotective properties, has emerged as a potential therapeutic target. Tongxinluo (TXL), a traditional Chinese medicine, mitigates MF by upregulating NRG-1. This study elucidates the mechanisms underlying the protective effects of NRG-1 and TXL against MF following AMI. Left anterior descending artery ligation established a model for mice with AMI. Adeno-associated virus was used to modulate NRG-1 expression in the myocardium. Echocardiography assessed cardiac function, and histological staining was used to evaluate MF. Expression levels of markers for myofibroblasts (α-SMA, FSP-1) and endothelial cells (CD31, VE-cadherin) were analysed to investigate EndMT. The involvement of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling pathway in NRG-1’s protective mechanism was validated using biochemical methods. Tongxinluo was administered to mice with AMI via gavage for 4 weeks, and its effects on cardiac function, MF and EndMT were assessed. Overexpression of NRG-1 in mice with AMI ameliorated cardiac dysfunction and reduced interstitial and perivascular fibrosis, whereas NRG-1 deficiency exacerbated these effects. NRG-1 protected against EndMT, as evidenced by changes in myofibroblast and endothelial cell markers. The PI3K/AKT signalling pathway was involved in NRG-1’s protective mechanism against MF. The administration of TXL to mice with AMI improved cardiac function and reduced MF by activating NRG-1. Furthermore, TXL inhibited EndMT post-AMI through the NRG-1/PI3K/AKT pathway. NRG-1 and TXL protect against MF post-AMI by mitigating EndMT through the PI3K/AKT pathway. These findings suggest that targeting NRG-1 or using TXL may be promising therapeutic strategies for MF following AMI.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10378-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and mechanism of inhibition of the GPR30-PI3K pathway by 4-phenylbutyric acid in the treatment of intrahepatic cholestasis of pregnancy","authors":"E. Liao,&nbsp;Qiao-Qiao Liu,&nbsp;Xiao-Mei Huang,&nbsp;Yong Shao","doi":"10.1007/s10735-025-10387-6","DOIUrl":"10.1007/s10735-025-10387-6","url":null,"abstract":"<div><p>Intrahepatic cholestasis of pregnancy (ICP) is a liver disease that manifests predominantly in the later stages of pregnancy. The primary treatment currently involves the use of ursodeoxycholic acid (UDCA). In this study, the therapeutic effectiveness of 4-phenylbutyric acid (4-PBA) in the treatment of ICP, as well as the potential mechanisms involved, are investigated to offer new references for clinical treatment decisions using ICP model. The therapeutic effect of 4-PBA on ICP was evaluated by drug therapy on ICP cells and animal models, and corresponding fluorescence immunoassay, electron microscope, WB and other experiments. In addition, the cells and animals treated with GPR30 inhibitor were treated to investigate whether 4-PBA promoted the expression of bile salt output pump (BSEP) protein through GPR30-PI3K pathway, thereby promoting bile acid excretion. Administration of 4-PBA significantly reduced the incidence of stillbirth associated with ICP. 4-PBA was effective in decreasing serum bile acid levels, reducing the activation of the GPR30-PI3K pathway, and increasing the expression of BSEP protein in hepatocytes. 4-PBA was effective in reducing bile acid levels and significantly improving fetal outcomes associated with ICP. The potential mechanism involves the promotion of BSEP localization and expression in the hepatocytes’ microvilli structures via the GPR30-PI3K pathway.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restore intestinal steady-state: new advances in the clinical management of chemotherapy-associated diarrhea and constipation","authors":"Miaoqi Chen,&nbsp;Yamao Li,&nbsp;Peijun Chen","doi":"10.1007/s10735-025-10367-w","DOIUrl":"10.1007/s10735-025-10367-w","url":null,"abstract":"<div><p>Chemotherapy remains the primary therapeutic strategy for most tumors, particularly those at advanced stages with distant metastases and resistance to molecularly targeted therapy or immunotherapy. There are many manifestations of chemotherapy-induced gastrointestinal toxicity (CIGT), including chemotherapy-induced diarrhea (CID) and chemotherapy-induced constipation (CIC). Although the World Health Organisation and the International Association Against Cancer have different grading criteria and strategies for the prevention and treatment of CIGT, there are still many unanswered questions that need to be clarified. This review critically describes pathological mechanisms and clinical research, analyzing the variability in diagnostic criteria and the absence of standardization in grading severity. We identify a critical gap in understanding the molecular underpinnings of CID and CIC and suggest targeted areas for future research, including developing personalized treatment approaches based on genetic profiling. The findings suggest a comprehensive treatment approach combining pharmacological and non-pharmacological strategies to enhance life quality and treatment adherence. This review will offer a comprehensive bird-eye of pathophysiological mechanisms, clinical manifestations, and therapeutic strategies of CIGT, thereby enriching accessible references to clinicians, and helping them to prevent and control CID and CIC.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10367-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of vincamine against ethanol-induced gastric ulcer by attenuation of IL-6, IL-1β, and TNF-α mRNA expression levels in the gastric mucosa of BALB/c mice","authors":"Hira Imam,&nbsp;Arham Shabbir,&nbsp;Anum Jamil,&nbsp;Adeel Masood Butt,&nbsp;Tabinda Fatima,&nbsp;Esraa M. Haji,&nbsp;Farhan K. Alswailmi,&nbsp;Ali F. Almutairy,&nbsp;Mujeeb Ur Rehman Parrey,&nbsp;Ashfaq Ahmad","doi":"10.1007/s10735-025-10374-x","DOIUrl":"10.1007/s10735-025-10374-x","url":null,"abstract":"<div><p>Vincamine, a monoterpenoid alkaloid, and an active constituent of plant <i>Catharanthus roseus</i> Linn, has been proclaimed for antioxidant and anti-inflammatory activities. This study was designed to evaluate the gastroprotective activity of Vincamine by ameliorating gastric ulcer in BALB/c mice. The study was also designed to find the possible mechanism of gastric protection by exploring the impact of Vincamine on gastric pH, acidic content, observing histopathology and molecular expression of inflammatory mediators like Interleukin- β (IL-1β), Interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF- α) and oxidative stress markers in the gastric tissue. A total number of 36 BALB/c mice were divided into 6 groups mainly normal control (NC) treated with normal saline, disease control (DC) treated with high dose of absolute ethanol (5ml/kg) while treatment groups involved pretreatment with low- dose Vincamine (VLD) at 10mg/kg body weight, medium-dose vincamine (VMD) at 20mg/kg body weight and high- dose vincamine (VHD) at 40mg/kg body weight before ethanol high dose administration and reference drug control, omeprazole (OMT) at the dose of 20 mg/kg body weight. Molecular expression levels of mRNA expressions of inflammatory cytokines like IL-1β, IL-6 and TNF- α were evaluated by using reverse transcription real time polymerase chain reaction method (RT-PCR). Pre-treatment of DC group with low (VLD), medium (VMD) and high doses (VHD) of vincamine improved gastric ulcer score and ameliorated histopathological parameter such as, infiltration of inflammatory cells, edema, fibrinoid necrosis, hemorrhage, and erosion score when compared to DC group. Induction of gastric model significantly increased (all P &lt; 0.05) the mRNA expression of IL-1β, IL-6 and TNF- α in the gastric tissue when same was compared to normal control group (NC). Pretreatment of DC group with different doses of vincamine (VLD, VMD and VHD) significantly downregulated (all P &lt; 0.05) the mRNA expressions of IL-1β, IL-6 and TNF- α and ameliorated oxidative stress marker MDA and increased antioxidant markers like SOD and GSH in the gastric tissue when same was compared to the DC group. In a nutshell, vincamine provide gastric protection in the BALB/c mice of gastric ulcer group by increasing the gastric pH, attenuated total acidity of the stomach and modulated infiltration of inflammatory cells, edema, fibrinoid necrosis, hemorrhage, and erosion score when compared to the DC group. Furthermore, vincamine possesses antiulcer and gastroprotective activity which may be ascribed to down-regulation the mRNA expression of IL-1β, IL-6 and TNF- α in the gastric tissue of disease control group. Vincamine also provide gastroprotective role by increasing the concentration of SOD and GSH while decreasing the MDA in gastric tissue.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143553672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of sufentanil on the proliferation, apoptosis, and epithelial-mesenchymal transition of ovarian cancer cells by regulating the SMAD3/SNAIL signaling pathway","authors":"Fei Zhao,&nbsp;Guiqing Liu,&nbsp;Lijuan Xiong,&nbsp;Liang Yao,&nbsp;Lijun Wang,&nbsp;Zheng Zhang","doi":"10.1007/s10735-025-10373-y","DOIUrl":"10.1007/s10735-025-10373-y","url":null,"abstract":"<div><p>To study sufentanil’s effect on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of ovarian cancer cells by modulating the SMAD3/SNAIL signaling pathway. Ovarian cancer A2780 cells were exposed to sufentanil at varying concentrations of 0 ng/mL, 20 ng/mL, 40 ng/mL, 60 ng/mL, 80 ng/mL, and 100 ng/mL. The proliferation of A2780 cells was assessed using the CCK-8 method; A2780 cells were randomly divided into three groups: CON group (normal culture), SUF group (60 ng/mL sufentanil intervention), and SUF + ACA group (60 ng/mL sufentanil and 100 ng/mL activin A intervention). After 48 h of culture, cell migration was evaluated by the scratch assay; Cell invasion was assessed using the Transwell chamber assay; Cell apoptosis was measured via flow cytometry; The growth status of the cells was observed under an optical microscope; The expression of N-cadherin, E-cadherin, SMAD3, TGF-β, and SNAIL proteins was detected by Western blot. When the concentration of sufentanil was ≥ 20 ng/mL, it dose-dependently inhibited the proliferation of ovarian cancer A2780 cells; In comparison to the CON group, the number of A2780 cells in the SUF group was significantly reduced, some cells detached, cell migration and invasion abilities, and the expression levels of N-cadherin, SMAD3, TGF-β, and SNAIL proteins decreased, while the apoptosis rate and E-cadherin protein expression levels increased (<i>P</i> &lt; 0.05); In comparison to the SUF group, the growth status of A2780 cells in the SUF + ACA group was good, cell migration and invasion abilities, and the expression levels of N-cadherin, SMAD3, TGF-β, and SNAIL proteins increased, while the apoptosis rate and E-cadherin protein expression levels decreased (<i>P</i> &lt; 0.05). Sufentanil may inhibit the proliferation and epithelial-mesenchymal transition of ovarian cancer cells and promote cell apoptosis by inhibiting the SMAD3/SNAIL signaling pathway.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143533099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}