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二氧化钛诱导的肝纤维化模型及白藜芦醇通过调节α-SMA和8-OHdG表达、氧化应激和炎症发挥的治疗作用。

Titanium dioxide-induced fibrotic liver model and the therapeutic effect of resveratrol by modulation of α-SMA and 8-oHdG expressions, oxidative stress, and inflammation.

作者信息

Başak Feyza, Kuşat Tansu, Ersan Yusuf, Kahraman Tahir

机构信息

Karabuk University, Faculty of Medicine, Department of Histology and Embryology, Karabuk, Turkey.

Karabuk University, Faculty of Medicine, Department of Histology and Embryology, Karabuk, Turkey.

出版信息

Tissue Cell. 2025 Apr;93:102748. doi: 10.1016/j.tice.2025.102748. Epub 2025 Jan 18.

Abstract

The research sought to assess the therapeutic impact of resveratrol by biochemical, immunohistochemical, and histopathological analyses in a TiO-induced liver fibrosis model. Titanium dioxide (100 mg/kg body weight) was delivered for 15 days to induce liver fibrosis, either alone or in conjunction with resveratrol (30 mg/kg body weight) therapy for the same duration. Resveratrol has been identified as a crucial therapeutic drug that provides an alternative treatment method for TiO-induced liver fibrosis by mitigating inflammation, oxidative stress, and the expressions of α-SMA and 8-OHdG. Resveratrol treatment mitigated TiO-induced liver fibrosis by repairing hepatocellular injury and decreasing plasma AST, ALT, and ALP levels. Resveratrol improves the activity of superoxide dismutase (SOD) and catalase (CAT), crucial enzymes for antioxidant defense, and elevates glutathione peroxidase (GSH-Px) levels, so augmenting antioxidant function. Furthermore, resveratrol decreased hepatic inflammation (IL-6 and IL-1β) and oxidative stress markers. Furthermore, histological alterations and immunohistochemistry expression of α-SMA and 8-OhdG were reinstated after resveratrol administration in the TiO-induced liver fibrosis model. Our research indicates that resveratrol administration effectively protects against liver fibrosis produced by TiO.

摘要

该研究旨在通过生化、免疫组织化学和组织病理学分析,评估白藜芦醇在二氧化钛诱导的肝纤维化模型中的治疗效果。给予二氧化钛(100毫克/千克体重)15天以诱导肝纤维化,单独给药或与白藜芦醇(30毫克/千克体重)联合给药相同时间。白藜芦醇已被确定为一种关键的治疗药物,通过减轻炎症、氧化应激以及α-SMA和8-OHdG的表达,为二氧化钛诱导的肝纤维化提供了一种替代治疗方法。白藜芦醇治疗通过修复肝细胞损伤和降低血浆AST、ALT和ALP水平,减轻了二氧化钛诱导的肝纤维化。白藜芦醇提高了超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性,这两种酶是抗氧化防御的关键酶,并提高了谷胱甘肽过氧化物酶(GSH-Px)水平,从而增强了抗氧化功能。此外,白藜芦醇降低了肝脏炎症(IL-6和IL-1β)和氧化应激标志物。此外,在二氧化钛诱导的肝纤维化模型中给予白藜芦醇后,α-SMA和8-OhdG的组织学改变和免疫组织化学表达恢复正常。我们的研究表明,给予白藜芦醇可有效预防二氧化钛引起的肝纤维化。

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