Human & experimental toxicology最新文献

Exploring the utility of zinc finger protein-related genes in predicting hepatocellular carcinoma prognosis, immune responses, and drug efficacy. 探讨锌指蛋白相关基因在预测肝癌预后、免疫反应和药物疗效中的应用。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-05-09 DOI: 10.1177/09603271251340277

Pengtao Zhai, Mei Li, Yuan Cheng

{"title":"Exploring the utility of zinc finger protein-related genes in predicting hepatocellular carcinoma prognosis, immune responses, and drug efficacy.","authors":"Pengtao Zhai, Mei Li, Yuan Cheng","doi":"10.1177/09603271251340277","DOIUrl":"https://doi.org/10.1177/09603271251340277","url":null,"abstract":"BackgroundHepatocellular carcinoma (LIHC), a prevalent liver cancer with a grim prognosis due to high recurrence rates, is under scrutiny for its association with zinc finger proteins (ZNFs) in tumorigenesis. This study aims to create a prognostic model for LIHC incorporating ZNF-related genes.MethodsBy analyzing TCGA data, we identified differentially expressed genes (DEGs) between normal and LIHC samples, focusing on ZNF-related genes through univariate Cox and LASSO Cox regression. A multivariate Cox regression model was built, categorizing LIHC patients into high- and low-ZNFRS groups based on ZNF-related risk scores. Model performance was evaluated using ROC curves, with a nomogram integrating clinical data and ZNFRS. Immune microenvironment, enrichment analysis, mutations, and drug responses in LIHC were also explored.ResultsA prognostic model utilizing 10 ZNF-related genes accurately predicted LIHC survival. The low-risk group exhibited enhanced immune cell infiltration, contrasting with cell cycle and DNA replication enrichment in the high-risk group, which also displayed increased mutation rates. Promising drug candidates like SNS-314 and Decitabine warrant further investigation in LIHC treatment.ConclusionThis study introduces impactful prognostic markers for LIHC management, emphasizing the significance of ZNFs in predicting patient outcomes and guiding treatment strategies.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251340277"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of concern. 表达关心。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271241310364

引用次数: 0

Whole transcriptome characterization of polystyrene microplastic-induced sperm DNA damage mouse spermatocytes model. 聚苯乙烯微塑料诱导精子DNA损伤小鼠精母细胞模型的全转录组特征。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-07-13 DOI: 10.1177/09603271251353491

Chenming Zhang, Zhelin Chen, Wenbang Liu, Sicheng Ma, Hangsai Chen, Yitong Xue, Qixin Pang, Jianshe Chen, Zixue Sun

{"title":"Whole transcriptome characterization of polystyrene microplastic-induced sperm DNA damage mouse spermatocytes model.","authors":"Chenming Zhang, Zhelin Chen, Wenbang Liu, Sicheng Ma, Hangsai Chen, Yitong Xue, Qixin Pang, Jianshe Chen, Zixue Sun","doi":"10.1177/09603271251353491","DOIUrl":"https://doi.org/10.1177/09603271251353491","url":null,"abstract":"ObjectiveTo explore the mechanisms by which microplastic toxicity leads to DNA damage in mouse spermatocytes.MethodsWe randomly divided GC-2 cells into a control group and a polystyrene microplastic (PS) group and then evaluated the DNA fragmentation index (DFI) in these cells via a comet assay. Whole-transcriptome sequencing was performed on the basis of DFI results. GO and KEGG enrichment analyses were based on the results of the entire transcriptome sequencing. At the same time, we also performed q-PCR validation on some significantly expressed genes and drew a toxicological network diagram on PS and mouse spermatocytes.ResultsComet assay results revealed that the intake of PS increased the DFI of mouse spermatocytes. Whole-transcriptome sequencing revealed that 61 circRNAs, 132 lncRNAs, 40 miRNAs, and 140 mRNAs were differentially expressed between the control and PS groups. GO and KEGG analyses revealed some notable enrichment in cellular components, molecular functions, biological processes, and gene expression pathways such as the defense response to viruses, the defense response to symbionts, the RIG-I-like receptor, the NOD-like receptor, and the calcium signaling pathways. Q-PCR and the network analysis revealed that PS affects the DFI of mouse spermatocytes mainly by influencing immune responses.ConclusionPS may damage the sperm DNA and increase the DFI by affecting cellular immunity-related pathways and redox pathways such as the RIG-I-like receptor and NOD-like receptor signaling pathways.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251353491"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144628336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Luteolin alleviates cyclophosphamide-induced premature ovarian failure in rats by regulating RNF8/HDAC2. 木犀草素通过调节RNF8/HDAC2减轻环磷酰胺诱导的大鼠卵巢早衰。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-06-24 DOI: 10.1177/09603271251350802

Ye Pan, Xiaoling Zeng, Xiaoting Rong, Yang Xu

{"title":"Luteolin alleviates cyclophosphamide-induced premature ovarian failure in rats by regulating RNF8/HDAC2.","authors":"Ye Pan, Xiaoling Zeng, Xiaoting Rong, Yang Xu","doi":"10.1177/09603271251350802","DOIUrl":"https://doi.org/10.1177/09603271251350802","url":null,"abstract":"ObjectiveThe study aimed to investigate the role of luteolin in alleviating POF and its underlying molecular mechanisms.MethodsPOF model was established in rats by intraperitoneal injection of 100 mg/kg cyclophosphamide. Then, rats in the treatment group received intragastric administration of with luteolin at doses of 25 mg/kg, 50 mg/kg and 100 mg/kg, respectively. Rats in POF model group were administered the same volume of saline intragastrically. The concentrations of E2, FSH, AMH, P, LH, SOD and MDA in serum were quantified using ELISA kits. H&E and TUNEL staining were employed to assess pathological alterations and apoptosis. The cellular localizations of 4-HNE, 8-OHdG and NTY were detected by immunohistochemistry staining. The PharmMapper database and UbiBrowser prediction were used for the prediction of luteolin interaction with RNF8/HDAC2.ResultsLuteolin treatment significantly increased serum levels of estradiol (E2) (P < 0.01) and anti-Müllerian hormone (AMH) (P < 0.01) while reducing follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels (P < 0.05), restoring ovarian function. Additionally, luteolin could significantly improve ovarian tissue morphology and reduce apoptosis. ELISA kit results indicated luteolin significantly reduced the levels of SOD and MDA. Immunohistochemical staining results revealed a significant decrease in the expressions of 4-HNE, 8-OHdG and NTY in luteolin treatment group. Combining The PharmMapper database and UbiBrowser prediction, we found luteolin could bind RNF8 and inhibit HDAC2 expression.DiscussionLuteolin could mitigate cyclophosphamide-induced ovarian senescence, with its molecular mechanisms involving the regulation of RNF8/HDAC2 signaling axis and the inhibition of oxidative stress.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251350802"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acriflavine protects against LPS-induced sepsis via regulation of pyroptosis, inflammation, and endoplasmic reticulum stress. 吖啶黄通过调节焦亡、炎症和内质网应激来防止脂多糖诱导的脓毒症。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-07-12 DOI: 10.1177/09603271251361194

Esraa G El-Waseif, Sara H Hazem, Dalia H El-Kashef, Ghada M Suddek

{"title":"Acriflavine protects against LPS-induced sepsis via regulation of pyroptosis, inflammation, and endoplasmic reticulum stress.","authors":"Esraa G El-Waseif, Sara H Hazem, Dalia H El-Kashef, Ghada M Suddek","doi":"10.1177/09603271251361194","DOIUrl":"https://doi.org/10.1177/09603271251361194","url":null,"abstract":"BackgroundLipopolysaccharide (LPS) is a glycolipid that constitutes the Gram-negative bacteria outermost membrane main portion. LPS is frequently of concern in medicine because of nearly all severe sepsis patients have elevated LPS plasma levels, which cause life-threatening organ dysfunction. Consequently, the potential protective benefit of acriflavine (Ac) in limiting LPS-induced acute inflammatory response and the possible underlying mechanisms were investigated.MethodsMale albino mice were treated with i.p. Ac 4 or 8 mg/kg/day for 2 weeks, then received a single i.p. LPS (10 mg/kg) at day 14.ResultsAc administration ameliorated hepatic, pulmonary, and testicular dysfunction, as confirmed by attenuation of pathological changes and amendment of oxidative stress parameters. This was associated with inhibition of protein kinase R-like endoplasmic reticulum kinase/phosphatidylinositol 3-kinase (PERK/PI3K) endoplasmic reticulum (ER) stress pathway; toll-like receptor 4/nuclear factor kappa B (TLR4/NF-κB) and active caspase-1/gasdermin D (GSDMD)-N-terminal as well as interleukin-1 beta (IL-1β) inflammatory and pyroptotic signals.ConclusionOur results highlighted the protective potential of Ac in a mouse model of LPS-mediated systemic inflammatory response, which paves the way for its clinical application in sepsis.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251361194"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Physalin A induces apoptosis through conjugating with Fas-FADD cell death receptor in human oral squamous carcinoma cells and suppresses HSC-3 cell xenograft tumors in NOD/SCID mice. Physalin A通过结合Fas-FADD细胞死亡受体诱导人口腔鳞癌细胞凋亡，抑制NOD/SCID小鼠HSC-3细胞异种移植瘤。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-04-16 DOI: 10.1177/09603271251335220

Fu-Shin Chueh, Sheng-Yao Hsu, Kuang-Chi Lai, Yi-Chung Liu, Ping-Chiang Lyu, Yueh-Hsiung Kuo, Yi-Ping Huang, Wen-Tsong Hsieh

{"title":"Physalin A induces apoptosis through conjugating with Fas-FADD cell death receptor in human oral squamous carcinoma cells and suppresses HSC-3 cell xenograft tumors in NOD/SCID mice.","authors":"Fu-Shin Chueh, Sheng-Yao Hsu, Kuang-Chi Lai, Yi-Chung Liu, Ping-Chiang Lyu, Yueh-Hsiung Kuo, Yi-Ping Huang, Wen-Tsong Hsieh","doi":"10.1177/09603271251335220","DOIUrl":"https://doi.org/10.1177/09603271251335220","url":null,"abstract":"IntroductionOral carcinoma cancer exhibits high global incidence and mortality. Physalin A (PA) was reported to induce programmed cell death in cancer cells. No study has yet investigated the influence of PA in oral squamous cell carcinoma. Herein, this study aims to explore PA-induced anti-cancer effects in human oral carcinoma.MethodsThis study used DNA gel electrophoresis and Annexin V/PI staining to detect DNA fragmentation and cell apoptosis. Western blotting and immunofluorescence analyzed protein expression. Flow cytometry measured Ca2+ release and mitochondrial membrane potential (∆Ψm). Moreover, molecular docking models predicted the molecular binding affinity.ResultsDNA gel electrophoresis and annexin V/PI staining confirmed PA-induced DNA fragmentation and apoptosis. Flow cytometry showed PA increased Ca2+ release and reduced ∆Ψm levels. PA activated cleaved caspase-3, -8, and -9, upregulated Bax and Bid, and downregulated Bcl-2. PA dose-dependently increased Fas (CD95/APO-1), apoptosis-inducing factor (AIF), and cytochrome c release in western blotting analysis. Confocal microscopy confirmed increased Bax, AIF, cleaved caspase-3, and Fas, with decreased Bcl-2. Molecular docking showed strong PA binding via hydrophobic interactions with the Fas-associated death domain (FADD). Compared with cisplatin, PA inhibited HSC-3 cell xenograft tumor growth in NOD/SCID mice.DiscussionWe reveal that PA binds to the Fas-FADD complex, inducing caspase-8 activation and triggering extrinsic and intrinsic mitochondria-dependent apoptosis in HSC-3 cells. It also suppresses HSC-3 cell xenograft tumors in NOD/SCID mice. These findings suggest PA as a potential anti-oral cancer agent in the future.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251335220"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhancing breast cancer treatment: Evaluating the efficacy of hyaluronic acid-coated tamoxifen-loaded solid lipid nanoparticles on MCF7 cells. 增强乳腺癌治疗：评估透明质酸包被负载他莫昔芬的固体脂质纳米颗粒对MCF7细胞的疗效。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271251322531

Niloufar Ghayoumipour, Hossein Ghafouri

{"title":"Enhancing breast cancer treatment: Evaluating the efficacy of hyaluronic acid-coated tamoxifen-loaded solid lipid nanoparticles on MCF7 cells.","authors":"Niloufar Ghayoumipour, Hossein Ghafouri","doi":"10.1177/09603271251322531","DOIUrl":"10.1177/09603271251322531","url":null,"abstract":"Introduction: Tamoxifen (TMX) shows promise in treating breast cancer, but it faces challenges such as poor solubility, instability, and incomplete release when targeting tumors. Additionally, TMX therapy's toxicity is a critical issue in breast cancer treatment. This study aimed to assess the impact of hyaluronic acid (HA)-coated TMX-loaded solid lipid nanoparticles (HA-TMX-SLNs) on MCF7 breast cancer cells.Methods: Solid lipid nanoparticles (SLNs) were prepared using hot homogenization. The HA-TMX-SLNs and TMX-SLNs were characterized and evaluated through transmission electron microscopy (TEM). Cytotoxicity was assessed using the MTT assay, and Western blot analysis was utilized to identify key factors in the cell cycle and apoptosis.Results: The nanoparticles (HA-TMX-SLNs) demonstrated approximately 55% loading efficiency after 100 h. HA-TMX-SLNs exhibited lower cytotoxicity in MCF7 cells compared to other treatments. Significant decreases in expression levels of cyclin-dependent kinase (CDK) 4, Cyclin D1, CDK2, and Bcl2 were observed after treatment with HA-TMX-SLNs, along with an increase in cleaved/procaspase-7.Discussion: The in vitro release study showed that HA-coated SLNs consistently released the drug into the media under controlled conditions. Furthermore, HA-TMX-SLNs exhibited cytotoxic effects, increasing apoptosis and inhibiting cancer cell proliferation. These findings suggest that HA-TMX-SLNs effectively deliver TMX to breast cancer cells.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251322531"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143461174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical and laboratory prognostic factors associated with methanol toxicity outcomes in patients at Tabriz Sina Hospital: A retrospective study. 与大不里士新浪医院患者甲醇中毒结果相关的临床和实验室预后因素：一项回顾性研究

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-07-18 DOI: 10.1177/09603271251358632

Sajjad Ahmadi, Ali Ostadi, Hadi Chitsazi, Hossein Alikhah

{"title":"Clinical and laboratory prognostic factors associated with methanol toxicity outcomes in patients at Tabriz Sina Hospital: A retrospective study.","authors":"Sajjad Ahmadi, Ali Ostadi, Hadi Chitsazi, Hossein Alikhah","doi":"10.1177/09603271251358632","DOIUrl":"https://doi.org/10.1177/09603271251358632","url":null,"abstract":"IntroductionMethanol toxicity is a significant health concern with potentially severe outcomes. This study aimed to investigate the prognostic factors of patients with methanol toxicity referred to Tabriz Sina Hospital.MethodsA descriptive-analytical retrospective study was conducted in methanol toxicity patients admitted in Tabriz Sina Hospital since 2019 to 2021. Demographic characteristics and management methods were extracted from the patients' medical records.ResultsPatients were predominantly male (91.3%) with a median age of 30-40 years. Winter accounted for 48.7% of cases. Coma (OR = 8.0, 95% CI: 3.2-19.9) and arrhythmia (OR = 5.5, 2.0-15.1) at admission, pH <7.1 (OR = 4.2, 2.0-8.9), elevated creatinine (OR = 1.3/mg/dL, 1.1-1.6), opiate co-use (OR = 2.8, 1.2-6.5), and delayed ethanol therapy (>3 h, OR = 2.3, 1.1-4.8) independently increased mortality risk. Bicarbonate, Eprex, and methylprednisolone reduced complications. Time from ingestion to admission (48-72 h) did not affect mortality, but delayed hemodialysis initiation worsened outcomes.ConclusionEarly presentation and providing early therapeutic modalities have a significant impact on the mortality rate and the patients' outcome.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251358632"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activation of SIRT3/AMPK/mTOR-mediated autophagy promotes quercetin-induced ferroptosis in oral squamous cell carcinoma. SIRT3/AMPK/ mtor介导的自噬激活促进槲皮素诱导的口腔鳞状细胞癌铁下垂。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271251323753

Jin Wang, Jia-Hui Yang, Di Xiong, Ling Chen

{"title":"Activation of SIRT3/AMPK/mTOR-mediated autophagy promotes quercetin-induced ferroptosis in oral squamous cell carcinoma.","authors":"Jin Wang, Jia-Hui Yang, Di Xiong, Ling Chen","doi":"10.1177/09603271251323753","DOIUrl":"10.1177/09603271251323753","url":null,"abstract":"Introduction: Quercetin has been reported to inhibit the growth of oral squamous cell carcinoma (OSCC), but the mechanism remains unclear. Therefore, our study aimed to investigate the involvement of sirtuin 3 (SIRT3) and the autophagy-dependent form of cell death, ferroptosis, in the pathogenesis of OSCC, and observe the impacts of quercetin on ferroptosis and SIRT3/AMPK/mTOR-mediated autophagy.Methods: SIRT3 knock out or overexpressing SCC15 cell line was generated, treated with indicated drugs, and malondialdehyde (MDA) and ROS levels were measured. Roles of SIRT3 in regulating autophagy-mediated ferroptosis were assessed by immunoprecipitation and Western blotting.Results: SIRT3 overexpression increased levels of MDA and ROS, reducing cell viability, and SIRT3 knockout produced the opposing effect. SIRT3 overexpression upregulated ATG16L1 expression and the conversion of LC3-Ⅰ to LC3-Ⅱ, triggering autophagy. Suppression of autophagy by ATG16L1 knockout impaired SIRT3-triggered ferroptosis. Use of an AMPK inhibitor antagonized the induction of ferroptosis by SIRT3 in SCC15 cells, indicating the involvement of the AMPK/mTOR pathway. Additionally, quercetin significantly increased the levels of SIRT3, p-AMPK, ATG16L1, and the ratio of LC3-Ⅱ/Ⅰ, but reduced cell viability and p-mTOR in SCC15 cells. Autophagy and AMPK inhibitors, or SIRT3 deletion significantly antagonized the impacts of quercetin on the autophagy-mediated ferroptosis in cancer cells.Discussion: SIRT3 overexpression activated the AMPK/mTOR pathway and triggered ATG16L1-mediated autophagy, promoting ferroptosis in SCC15 cells, and we proposed that quercetin may be a promising therapeutic drug for OSCC.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251323753"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Protective effects of Tribulus Terrestris extract on cisplatin-induced ovarian damage: Antioxidants and anti-inflammatory insights. 蒺藜提取物对顺铂诱导的卵巢损伤的保护作用：抗氧化剂和抗炎见解。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-07-18 DOI: 10.1177/09603271251353492

Morteza Abdi, Hadi Karimzadeh, Amirreza Jourabchi, Abbas Majdi Seghinsara, Laleh Khodaie

{"title":"Protective effects of Tribulus Terrestris extract on cisplatin-induced ovarian damage: Antioxidants and anti-inflammatory insights.","authors":"Morteza Abdi, Hadi Karimzadeh, Amirreza Jourabchi, Abbas Majdi Seghinsara, Laleh Khodaie","doi":"10.1177/09603271251353492","DOIUrl":"https://doi.org/10.1177/09603271251353492","url":null,"abstract":"BackgroundCisplatin (CIS) is a widely used chemotherapeutic agent; however, it is associated with ovarian toxicity. Tribulus Terrestris (TT) is recognized for its antioxidant and anti-inflammatory properties. This study aims to evaluate the effects of TT extract on ovarian tissue damage induced by cisplatin.Material and MethodTwenty-five female BALB/c mice were divided into five groups (n = 5): Control, CIS (Cisplatin only), CIS + TT100 (100 mg/kg TT extract daily + CIS), CIS + TT300 (300 mg/kg TT + CIS), and CIS + TT500 (500 mg/kg TT daily + CIS). After 15 days, blood samples were collected for hormonal analysis, and ovaries were harvested for histopathological, immunohistochemical, and biochemical assessments.ResultsThe CIS group exhibited a significant decline in follicle count compared to the control group (P < 0.001). In contrast, the CIS + TT groups showed a notable increase in follicle count (P < 0.05). TT treatment also resulted in significant improvements in antioxidant markers (SOD, CAT) and a reduction in oxidative stress (MDA) compared to the CIS group. Moreover, E2, AMH, and progesterone concentrations were decreased in the CIS group, while these levels were restored in the TT-treated groups (P < 0.001). The expression of inflammatory markers TNF-α and IL-1β was higher in the CIS group and decreased in the TT-treated groups.ConclusionTribulus Terrestris extract effectively mitigates cisplatin-induced ovarian toxicity by enhancing follicular count, improving antioxidant activity, and reducing oxidative stress. TT treatment also elevated AMH and progesterone levels while decreasing inflammatory markers, underscoring its potential as a protective agent against cisplatin-induced ovarian damage.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251353492"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0