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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The protective effect of vildagliptin in chronic experimental cyclosporine A-induced hepatotoxicity
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The protective effect of vildagliptin in chronic experimental cyclosporine A-induced hepatotoxicity

机译：Vildaglitin在慢性实验环孢菌素A诱导的肝毒性的保护作用

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摘要

The study examined the effect of dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, in cyclosporine (CsA)-induced hepatotoxicity. Rats were divided into 4 groups treated for 28 days: control (vehicle), vildagliptin (10 mg/kg, orally), CsA (20 mg/kg, s.c.), and CsA-vildagliptin group. Liver function was assessed by measuring serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (gamma GT), lactate dehydrogenase (LDH), and albumin, and histopathological changes of liver were examined. Oxidative stress markers were evaluated. Assessment of nuclear factor-kappa B (NF-kappa B) activity in hepatic nuclear extract, serum DPP-4, and expression of Bax and Bcl2 were also done. CsA-induced hepatotoxicity was evidenced by increase in serum levels of AST, ALT, and gamma GT; a decrease in serum albumin; and a significant alteration in hepatic architecture. Also, significant increase in thiobarbituric acid reactive substance (TBARS) and decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) levels, increased expression Bax proteins with deceased expression of Bcl2, and increased hepatic activity of NF-kappa B and serum DPP-4 level were observed upon CsA treatment. Vildagliptin significantly improved all altered parameters induced by CsA administration. Vildagliptin has the potential to protect the liver against CsA-induced hepatotoxicity by reducing oxidative stress, DPP-4 activity, apoptosis, and inflammation.
机译：该研究检测了二肽肽肽酶-4（DPP-4）抑制剂，Vildagliptin，在环孢菌素（CSA）诱导的肝毒性的作用。将大鼠分为4组处理28天：对照（载体），Vildagliptin（10mg / kg，口服），CSA（20mg / kg，S.C.）和CSA-Vildagliptin组。通过测量血清水平的天冬氨酸氨基转移酶（AST），丙氨酸氨基转移酶（ALT），γ谷氨酰胺转移酶（γGT），乳酸脱氢酶（LDH）和白蛋白以及肝脏的组织病理学变化来评估肝功能。评估氧化应激标记物。还进行了评估肝核提取物，血清DPP-4和BAX和BCL2表达的核因子-Kappa B（NF-Kappa B）活性。 CSA诱导的肝毒性通过血清AST，ALT和Gamma GT的增加证明了肝毒性。血清白蛋白减少;和肝脏建筑的显着改变。此外，硫氨基吡咯酸反应物质（TBARS）的显着增加和超氧化物歧化酶（SOD），过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GPX）和谷胱甘肽（GSH）水平的降低，表达Bax蛋白与已故的BCl2表达，和在CSA治疗时观察到NF-Kappa B和血清DPP-4水平的增加的肝脏活性。 Vildagliptin显着改善了CSA给药诱导的所有改变的参数。 Vildagliptin具有通过降低氧化应激，DPP-4活性，凋亡和炎症来保护肝脏诱导CSA诱导的肝毒性。

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