Tissue & cell最新文献

{"title":"Altered lung inflammation and expression of endoplasmic reticulum stress markers in male mice aged-asthma model.","authors":"Farshad Armin, Hamdollah Panahpour, Ramin Salimnejad, Hakimeh Saadati, Ali Abedi, Mohammad Reza Aslani","doi":"10.1016/j.tice.2025.102938","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102938","url":null,"abstract":"<p><p>Although there is a strong correlation between aging and asthma pathophysiology, the underlying mechanism has not been fully elucidated. The endoplasmic reticulum (ER) has been demonstrated to be a crucial intracellular organelle involved in the pathogenesis of numerous diseases. The aim of the current study was to investigate ER stress markers in the lung tissue of aged ovalbumin (OVA)-sensitized mice. Male BALB/C mice were randomly divided into the following four groups (10 in each): 1) control, 2) OVA-sensitized (OVA), 3) D-galactose-induced aging (D-gal), and 4) OVA-sensitized associated with D-galactose-induced aging (OVA+D-gal). Total WBCs and differential cells were counted using the bronchoalveolar lavage (BAL) fluid. Lung tissue was analyzed for ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) through Real Time-PCR technique as well as histopathological assessment. The data indicated a significant increase in both total WBCs and differential cells within the OVA, D-gal, and OVA+D-gal groups when compared to the control group, particularly evident in the OVA+D-gal group. Also, the results showed that the increased expression of ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) was significantly higher in the OVA, D-gal, and OVA+D-gal groups than in the control group. Interestingly, the increased expression of CHOP, ATF4, and XBP1 was observed in the OVA+D-gal group more than in other groups. In aged OVA-sensitized mice, the findings revealed a maladaptive ER stress response in their lung tissue, characterized by elevated levels of CHOP, ATF4, and XBP1 expression.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"102938"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050074","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":"Exercise ameliorates cardiac injury induced by nandrolone decanoate through downregulation of osteopontin and mTOR expressions.","authors":"Mohamed Aref, Wesam Mr Ashour, Nanees F El-Malkey, Haifa A Alqahtani, Mohamed A Nassan, Noha Ali Abd-Almotaleb, Gamal A Salem","doi":"10.1016/j.tice.2025.102932","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102932","url":null,"abstract":"<p><p>Nandrolone-decanoate (NA), a synthetic anabolic steroid, negatively impacts cardiac function. While exercise is known to benefit cardiovascular health, its effects on individuals misusing anabolic steroids require further study. Osteopontin (OPN) and mammalian target of rapamycin (m-TOR) are crucial in inflammation-related cardiovascular diseases and can be influenced by exercise, though results are inconclusive. This study aims to examine how exercise affects NA's cardiac adverse effects and the potential role of OPN and m-TOR. The study involved 52 male rats divided into four groups: control, exercise-only, NA-treated (15 mg/kg/day S.C for 8 W), and combined exercise and NA treatment. Researchers measured blood pressure, heart rate (HR), serum cardiac enzymes, CRP, IL-1B, IL-6, Brain Natriuretic Peptide (BNP) and conducted macro and micromorphological assessments. Additionally, immunohistochemical analysis of cardiac OPN and mTOR was performed. The NA-treated group showed significant increases in blood pressure, HR, weight, and cardiac enzymes compared to the control group. Exercise significantly improved these parameters in the combined exercise and NA treatment group, except for blood pressure. All groups exhibited an increase in cardiac weight relative to the control. The NA-treated group displayed marked hyaline degeneration and necrosis in cardiac tissues, with increased cell diameter and excess collagen deposition, which was less severe in the combined exercise (EX) and NA treatment group. NA treatment significantly elevated inflammatory mediators and the area percentage of OPN and m-TOR expression. These markers were significantly reduced in the combined exercise and NA treatment group. BNP was remarkably raised in EX+NA group compared to all other groups. Exercise mitigated NA-induced cardiac damage by reducing inflammation, possibly through the downregulation of cardiac OPN and m-TOR expression.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"102932"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033183","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":"Impacts of type 1 diabetes mellitus on male fertility and embryo quality in superovulated mice.","authors":"Begum Alyürük, Yusufhan Yazir, Zeynep Ece Utkan Korun, Özcan Budak, Ender Yalçinkaya Kalyan, Kamil Can Kiliç","doi":"10.1016/j.tice.2025.102941","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102941","url":null,"abstract":"<p><strong>Objective: </strong>We aimed to compare embryo quality, sperm morphology, motility, and fertilization obtained from male mice with type 1 diabetes mellitus (T1DM) induced by streptozotocin (STZ) in control and diabetic mice undergoing in vitro fertilization (IVF).</p><p><strong>Methods: </strong>CD-1 male mice were divided into control and DM groups, with an i.p. injection of 100 mg/kg STZ to induce T1DM. One month later, the mice were euthanized to investigate the effects of STZ-induced T1DM on the reproductive system. Sperms were obtained from the epididymis and vas deferens. The morphology and motility of the cells were evaluated. Follicle development was stimulated by controlled ovarian stimulation, and oocytes were collected by extracting oviducts and ovaries from female mice housed under controlled environmental conditions with ad libitum access. Both groups underwent IVF with fertilized zygotes followed up until the third day before embryo quality was compared.</p><p><strong>Results: </strong>Female mice bred with diabetic males exhibited significantly lower fertilization rates than the controls (p < 0.05). Sperm from diabetic mice displayed abnormalities in shape and movement, with reduced motility and fertilization. Embryos from male diabetic mice exhibited a higher incidence of developmental arrest during early embryogenesis. Although no significant differences in oocyte quality were observed, embryos from diabetic mice exhibited higher growth rates. These findings highlighted the T1DM's detrimental effects on sperm morphology, motility, fertilization, and early embryonic development, thus contributing to our understanding of reproductive complications.</p><p><strong>Conclusion: </strong>In conclusion, our findings demonstrated that T1DM significantly impaired sperm morphology, motility, and fertilization capacity, leading to reduced embryo quality and increased developmental arrest. These results highlight the detrimental impact of DM on male reproductive potential and underscore the importance of glycemic control in optimizing outcomes in assisted reproductive techniques such as IVF.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"102941"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033184","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":"Flavonoid-rich Deverra tortuosa extract mitigates ethanol-induced gastritis via modulation of cytokine networks, oxidative pathways, and mucosal immunotoxicity","authors":"Mohamed F. Abdelhameed ,&nbsp;Mosab Gad ,&nbsp;Heba A.S. El-Nashar ,&nbsp;Rehab F. Taher ,&nbsp;Rehab F. Abdel-Rahman ,&nbsp;Asmaa S. Abd Elkarim ,&nbsp;Alaa M. Ali ,&nbsp;Mohamed A. Farag ,&nbsp;Abdelsamed I. Elshamy","doi":"10.1016/j.tice.2025.103067","DOIUrl":"10.1016/j.tice.2025.103067","url":null,"abstract":"<div><div>Gastric ulcers are a major gastrointestinal disorder influenced by environmental and lifestyle factors, warranting for the discovery of effective therapeutic alternatives. <em>Deverra tortuosa</em> (Desf.) DC., a traditional medicinal plant, has demonstrated potential gastroprotective properties. This study assesses the anti-ulcerative effects of phenolic-rich ethanolic extract of <em>D. tortuosa</em> (DT-ETOH) against ethanol-induced gastritis in rats, alongside its underlying mechanisms of action. Comprehensive metabolites profiling via UHPLC-ESI-qTOF-MS/MS identified 35 bioactive compounds, primarily flavonoids and phenolic acids, along with coumarins, sterols, and fatty acids. Oral administration of DT-ETOH significantly mitigated gastric ulceration by reducing the ulcer index and oxidative stress markers, enhancing antioxidant enzyme activity (SOD, GSH), and modulating key inflammatory mediators (TNF-α, IL-6). Notably, DT-ETOH administration led to the upregulation of Keap-1 and HO-1 expression, increased iKba levels, and suppression of iNOS, indicating its role in oxidative stress regulation and inflammation suppression. Histopathological findings further confirmed the protective effects of DT-ETOH, demonstrating improved gastric mucosal integrity. These results provide evidence of DT-ETOH's gastroprotective, antioxidant, and anti-inflammatory properties, supporting its potential as a natural agent for gastric ulcer management.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103067"},"PeriodicalIF":2.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757667","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":"Alterations of matrisome gene expression in multipotent mesenchymal stromal cells under physiological hypoxia in vitro","authors":"Diana Matveeva ,&nbsp;Elena Andreeva,&nbsp;Yulia Rudimova,&nbsp;Aleksandra Gornostaeva,&nbsp;Danila Yakubets,&nbsp;Irina Andrianova,&nbsp;Ludmila Buravkova","doi":"10.1016/j.tice.2025.103064","DOIUrl":"10.1016/j.tice.2025.103064","url":null,"abstract":"<div><div>Low O₂ level (physiological hypoxia) is an important physical parameter in local tissue niches of multipotent mesenchymal stromal cells (MSCs). Hypoxia preconditioning is actively applied in cell therapy and regenerative medicine protocols. In the present study, the effect of physiologic hypoxia <em>in vitro</em> (5 % O₂) on the extracellular matrix of MSCs from the stromal-vascular fraction of human adipose tissue was investigated. Compared to standard cell culture conditions (20 % O₂), the genes encoding structural and regulatory proteins of the extracellular matrix (matrisome) were differentially expressed in MSCs under physiologic hypoxia. There was a significant downregulation of genes coding structural glycoproteins (<em>COMP, ELN</em>) in the core matrisome and upregulation of genes encoded matrisome-associated proteins with pro-migratory (<em>CXCL12</em>) and antioxidant (<em>SRPX, SERPINF1</em>) functions. At different O₂ levels, there were no significant differences in immunocytochemically identified the core matrisome proteins: collagen I, fibronectin, osteonectin, versican, nor in the expression of the corresponding genes. Meanwhile, variations in packaging patterns of the fibrils were, however, demonstrated using scanning electron microscopy. Under 5 % O₂ the activities of the soluble matrix metalloproteinases MMP-1 and MMP-2 were reduced. Thus, physiological hypoxia modulates the matrisome properties, and understanding this may be important for gaining mechanistic insights into the activity of MSCs in local tissue microenvironments, as well as in the protocols for scaffold production based on native ECMs for use in regenerative medicine.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103064"},"PeriodicalIF":2.5,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757520","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":"A collagen-based amniotic membrane scaffold combined with photobiomodulation accelerates wound repair in diabetic rats through modulation of inflammation and tissue regeneration","authors":"Ahmed Hjazi","doi":"10.1016/j.tice.2025.103063","DOIUrl":"10.1016/j.tice.2025.103063","url":null,"abstract":"<div><div>Chronic diabetic wounds present significant challenges to effective tissue repair due to persistent inflammation and impaired regeneration. In this study, we investigated the therapeutic potential of a bioengineered collagen scaffold derived from the human amniotic membrane (CSAM), used alone or in combination with photobiomodulation therapy (PBMT), in a diabetic rat wound model. Forty diabetic rats were allocated into four groups: control, CSAM, PBMT, and CSAM+PBMT. Wound healing was assessed on days 4 and 8 post-injury. Combined treatment (CSAM+PBMT) significantly enhanced wound closure and histological regeneration, with notable increases in fibroblast and blood vessel density, epidermal and dermal thickness, collagen deposition, and expression levels of VEGF and bFGF compared to other groups. Additionally, this group exhibited a marked reduction in neutrophil infiltration and pro-inflammatory cytokines, including IL-1β, TNF-α, and NF-κB. These results demonstrate that the synergistic application of PBMT and CSAM fosters a pro-regenerative wound microenvironment by suppressing inflammation and promoting cellular proliferation and extracellular matrix remodeling. This combinatory approach offers a promising therapeutic avenue for improving diabetic wound healing outcomes.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103063"},"PeriodicalIF":2.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739533","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":"ELAVL1 promotes ferroptosis-induced inhibition of osteogenic differentiation in diabetic osteoporosis by downregulating SIRT1","authors":"Bi Huang ,&nbsp;Jie Jiang ,&nbsp;Xiang Ou ,&nbsp;Meng Hao ,&nbsp;Huige Shao","doi":"10.1016/j.tice.2025.103060","DOIUrl":"10.1016/j.tice.2025.103060","url":null,"abstract":"<div><h3>Objective</h3><div>Ferroptosis can implicate in the pathogenesis of diabetic osteoporosis (DOP). This study aimed to determine whether Sirtuin 1 (SIRT1) modulates DOP through ELAV-like RNA binding protein 1 (ELAVL1)-mediated ferroptosis.</div></div><div><h3>Methods</h3><div>MC3T3-E1 cells were cultured in high glucose (HG) medium, and osteogenic differentiation was assessed by evaluating RUNX2, OCN, ALP activity, and calcium deposition via Alizarin Red S staining. Ferroptosis was evaluated by measuring GPX4, ACSL4, ROS, MDA, and Fe^2 + . A DOP mouse model was established using C57BL/6 J mice fed a high-fat diet combined with 1 % streptozotocin injection. Femoral histopathology, body weight, fasting blood glucose (FBG), and ferroptosis were analyzed.</div></div><div><h3>Results</h3><div>HG exposure inhibited osteogenic differentiation, characterized by the reduction in RUNX2, OCN ALP activity and calcium accumulation in MC3T3-E1 cells (<em>P</em> &lt; 0.05); it induced ferroptosis, including the decrease in GPX4 and the increase in ACSL4, ROS, MDA and Fe²⁺ (<em>P</em> &lt; 0.05). SIRT1 overexpression or treatment with Fer-1 reversed HG-induced ferroptosis and restored osteogenic differentiation (<em>P</em> &lt; 0.05). SIRT1 was shown to bind ELAVL1, and its overexpression suppressed ELAVL1(<em>P</em> &lt; 0.05). In HG-stimulated cells co-overexpressing SIRT1 and ELAVL1, both ferroptosis and osteogenic markers resembled those in cells exposed to HG (<em>P</em> &lt; 0.05). DOP mice exhibited elevated FBG, reduced body weight, increased ELAVL1, and decreased SIRT1(<em>P</em> &lt; 0.05); these mice showed impaired femoral histology. Ferroptosis was evident in DOP mice (<em>P</em> &lt; 0.05). Silencing ELAVL1 improved femoral tissue integrity, inhibited ferroptosis, promoted osteogenic differentiation, restored body weigh, and upregulated SIRT1 in DOP mice (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>ELAVL1 repressed SIRT1 translation to interrupt ferroptosis-mediated osteoblastic differentiation, thereby inhibiting DOP progression.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103060"},"PeriodicalIF":2.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757521","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":"A combined therapeutic approach: Parthenolide and vincristine modulate autophagy in B-cell acute lymphoblastic leukemia","authors":"Elmira Zarei ,&nbsp;Sepide Namdari ,&nbsp;Farahnaz Zare ,&nbsp;Gholamreza Rafiei Dehbidi ,&nbsp;Mansoureh Nazari ,&nbsp;Gholamhossein Tamaddon ,&nbsp;Azadeh Omidkhoda","doi":"10.1016/j.tice.2025.103057","DOIUrl":"10.1016/j.tice.2025.103057","url":null,"abstract":"<div><h3>Background</h3><div>Parthenolide (PTL), derived from <em>Tanacetum parthenium</em>, is known for its anti-inflammatory and anti-cancer properties, primarily through NF-κB inhibition and modulation of reactive oxygen species. This study investigates PTL's potential as a complementary treatment for B-Cell Acute Lymphoblastic Leukemia, focusing on its effects on autophagy, apoptosis, and proliferation in the Nalm-6 cell line, alongside vincristine, with the aim of addressing challenges such as multi-drug resistance.</div></div><div><h3>Methods</h3><div>Nalm-6 cells were treated with increasing concentrations of PTL and VCR to determine their IC50 values, followed by combination treatments with sub-IC50 doses. Apoptosis was assessed using flow cytometry, while changes in autophagy-related gene expression (BECN1, ATG10, LC3, and P62) were measured via Real-time PCR, and LC3 protein levels were analyzed through Immunoblotting.</div></div><div><h3>Results</h3><div>The results revealed that both PTL and VCR inhibited Nalm-6 cell proliferation in a concentration and time-dependent manner, with a synergistic effect observed in combined treatments. This combination also increased apoptosis and significantly enhanced the expression of autophagy-related genes ATG10, LC3 and BECN1 while decreasing P62 expression. Additionally, VCR and PTL increased LC3B-II protein levels.</div></div><div><h3>Conclusion</h3><div>Overall, the study indicates that combined treatment promotes autophagy and apoptosis, suggesting that PTL could be a beneficial adjunct to chemotherapy for treating B-ALL in the future.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103057"},"PeriodicalIF":2.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739531","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":"IMUP promotes fatty acid metabolism and lung cancer progression by regulating TGF-β/SMAD3 signaling pathway","authors":"Shuang Wu ,&nbsp;Feiyu Liu ,&nbsp;Xiangwen Yao ,&nbsp;Yiming Lei ,&nbsp;Wei Wang","doi":"10.1016/j.tice.2025.103061","DOIUrl":"10.1016/j.tice.2025.103061","url":null,"abstract":"<div><h3>Purpose</h3><div>The purpose of this study was to investigate the biological role of immortalization-upregulated protein (IMUP) in lung cancer.</div></div><div><h3>Methods</h3><div>Through bioinformatics analysis, IMUP expression in lung cancer tissues, overall survival (OS) of patients with lung cancer, and the biological pathways related to IMUP were analyzed. IMUP expression was assessed utilizing immunohistochemistry staining, RT-qPCR, and western blot. Lung cancer cells’ biological behaviors were determined through flow cytometry, CCK-8, EdU, wound healing, and transwell assays. IMUP’s influences on lipid content were assessed using BODIPY 493/503 staining. Western blot was utilized for checking the changes of epithelial-mesenchymal transition (EMT) related proteins (E-cadherin, N-cadherin, Slug, and Vimentin), some key lipid metabolism proteins (FASN, ACC, and ACSS2) and proteins related to TGF-β signaling pathway (TGF-β, SMAD3, and p-SMAD3). The mouse xenograft model was established to evaluate IMUP’s role in lung cancer growth in vivo.</div></div><div><h3>Results</h3><div>In lung cancer tissues and cells, the upregulated IMUP was observed. Patients with high IMUP expression displayed a poorer OS. IMUP knockdown inhibited lung cancer cell proliferation, viability, migration, invasion, and EMT, but induced cell apoptosis. Lower lipid content and the levels of FASN, ACC, and ACSS2 were observed in lung cancer cells with downregulated IMUP. However, the above malignant biological behaviors displayed the contrary results in lung cancer cells with upregulated IMUP. Notably, IMUP overexpression increased TGF-β and p-SMAD3/SMAD3 expression. On the contrary, IMUP knockdown inhibited TGF-β and p-SMAD3/SMAD3 expression. Besides that, the suppression of IMUP knockdown on lung cancer cell proliferation, invasion, and fatty acid metabolism was reversed by TGF-β, the promotive effects of IMUP overexpression on cell proliferation, invasion, and fatty acid metabolism were reversed by SIS3 (a SMAD3 inhibitor). In vivo, IMUP knockdown suppresses lung cancer growth, increased E-cadherin expression, and decreased the expression of Ki67, N-cadherin, FASN, ACC, and TGF-β.</div></div><div><h3>Conclusion</h3><div>IMUP knockdown inhibited TGF-β/SMAD3 signaling pathway, thereby restraining fatty acid metabolism and lung cancer progression.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103061"},"PeriodicalIF":2.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739532","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":"Cardioprotective effect of Cymbopogon proximus and febuxostat on venlafaxine induced subacute cardiotoxicity in adult male Albino rats: Histological and immunohistochemical study","authors":"Marwa M. Hassan ,&nbsp;Basma H. Amin ,&nbsp;Mohammed Yosri ,&nbsp;Heba Bayoumi ,&nbsp;Hosam M. Aly ,&nbsp;Eman A. El-Sawaf","doi":"10.1016/j.tice.2025.103056","DOIUrl":"10.1016/j.tice.2025.103056","url":null,"abstract":"<div><div><strong>Cardiotoxicity</strong> linked to the commonly prescribed antidepressant venlafaxine represents a major worldwide clinical challenge and patient safety concern. There is a pressing need for efficient interventions because there are currently no recognized protective agents that specifically target venlafaxine-induced cardiac damage. <em>Cymbopogon proximus</em> is a natural plant whose extract contains antioxidants and anti-inflammatory properties. Febuxostat, a xanthine oxidase inhibitor, exhibits anti-inflammatory, antioxidant, and immune-modulating impact beyond its primary use, suggesting potential for repurposing. This investigation critically evaluates the efficiency of <em>C. proximus</em> extract and febuxostat in protection against venlafaxine-induced subacute cardiac damage to address this critical gap. 72 rats in 6 groups: I (control); II (<em>C. proximus</em> 800 mg/kg, daily oral gavage); III (febuxostat 10 mg/kg, daily oral gavage); IV (venlafaxine 50 mg/kg via oral gavage every 10 days for 30 days); V (venlafaxine + <em>C. proximus</em>); VI (venlafaxine + febuxostat). After 30 days of treatment, the rats were euthanized for testing. The groups treated with <em>C. proximus</em> extract or febuxostat exhibited much higher survival rates among rats that were affected by venlafaxine toxicity. These treatments effectively restored cardiac indices to near-normal levels and attenuated pathological alterations, evidenced by reduced nuclear positivity of PCNA staining, significant decreases in pro-inflammatory markers, increased redox indicators, and downregulation of key mediators: fibrosis driver TGF-β, cardiac stress marker BNP, along with Collagen-α1 and MMP2. Furthermore, levels of ALT, AST, creatinine, and BUN were maintained within normal ranges in the treated groups. These data demonstrate that <em>C. proximus</em> extract and febuxostat confer significant cardioprotective effects against venlafaxine-induced subacute cardiac toxicity, primarily mediated via their antioxidant and anti-inflammatory properties.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103056"},"PeriodicalIF":2.5,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144750199","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}