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Magnesium isoglycyrrhizinate shows hepatoprotective effects in a cyclophosphamide-induced model of hepatic injury

机译:异甘草酸镁在环磷酰胺诱导的肝损伤模型中显示出肝保护作用

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摘要

The purpose of the current study was to investigate the effect of Magnesium Isoglycyrrhizinate (GM) on cyclophosphamide (CP)-induced hepatic injury in vivo and in vitro. The results demonstrated that GM exerted a protective effect on CP-induced acute liver injury, as evidenced by the alleviations of hepatic pathological damage and serum transaminase activities. Meantime, GM attenuated serum and HepG2 cell supernatant levels of TNF-α, IL-6, IL-1β, SOD and MDA. Western blot results presented that GM down-regulated the expressions of the microtubule associated protein 1A/1B-light chain 3 (LC3), Lysosome associated membrane protein-1 (LAMP-1), p-phosphatidylinositol 3-kinase (PI3K), p-protein Kinase B(Akt), p-mechanistic target of rapamycin(mTOR), p-ribosomal protein S6 kinase 70 kDa (p70S6K), p-4E binding protein 1(4EBP1), p- inhibitor of NF-κB(IκB)α and p-nuclear factor kappa B(NF-κB)p65 in CP-stimulated hepatic tissue and HepG2 cells. Taken together, our results suggested that GM showed beneficial effect on CP-induced liver injury through NF-κB-mediated inflammation and PI3K/Akt/mTOR/p70S6K/4EBP1 axis-mediated autophagy in vivo and in vitro.
机译:本研究的目的是在体内和体外研究异甘草酸镁(GM)对环磷酰胺(CP)诱导的肝损伤的影响。结果表明,GM对CP诱发的急性肝损伤具有保护作用,这可以通过减轻肝脏病理损伤和血清转氨酶活性来证明。同时,GM减弱了血清和HepG2细胞上清液中TNF-α,IL-6,IL-1β,SOD和MDA的水平。 Western印迹结果表明,GM下调了微管相关蛋白1A / 1B-轻链3(LC3),溶酶体相关膜蛋白-1(LAMP-1),对磷脂酰肌醇3-激酶(PI3K),p的表达-蛋白激酶B(Akt),雷帕霉素(mTOR)的p机制靶标,p-核糖体蛋白S6激酶70 kDa(p70S6K),p-4E结合蛋白1(4EBP1),p-NF-κB(IκB)抑制剂CP刺激的肝组织和HepG2细胞中的α和p核因子κB(NF-κB)p65。两者合计,我们的结果表明,GM在体内和体外通过NF-κB介导的炎症和PI3K / Akt / mTOR / p70S6K / 4EBP1轴介导的自噬对CP诱导的肝损伤显示出有益的作用。

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