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首页> 外文期刊>American Journal of Physiology >S-allyl-glutathione improves experimental liver fibrosis by regulating Kupffer cell activation in rats
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S-allyl-glutathione improves experimental liver fibrosis by regulating Kupffer cell activation in rats

机译：S-烯丙基 - 谷胱甘肽通过调节大鼠Kupffer细胞活化来改善实验性肝纤维化

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摘要

S-allyl-gluta-thione (SAG) is one of the metabolites of diallyl sulfide (DAS), a component of garlic. DAS has shown preventative effects on carci-nogenesis in animal models. However, whether synthetic SAG can improve liver fibrosis has not been investigated. We examined the potential preventive effects of SAG on acute and chronic models of liver fibrosis by chronic carbon tetrachloride (CCU) administration. SAG inhibited liver fibrogenesis induced by CCU in a dose-dependent manner and reduced heat shock protein-47 (HSP47), a collagen-specific chaperone, and other fibrosis markers. In fibrosis regression models, after administration of either CC1_4 for 9 wk or dimethyl nitrosamine (DMN) for 6 wk, SAG markedly accelerated fibrolysis in both models. In the regression stage of DMN-treated liver, SAG normalized the ratio of M2 phenotype (expression of mannose receptor) in Kupffer cells (KCs). Consistent with these results, the culture supematants of SAG-treated M2-phenotype KCs inhibited collagen-α1 (I) chain (COL1A1) mRNA expression in primary culture-activated rat hepatic stellate cells (HSCs). However, SAG did not directly inhibit HSC activation. In an acute model of CC1_4 single injection, SAG inhibited hepatic injury dose dependently consistent with the inhibited the elevation of the bilirubin and ALT levels. These findings suggest that SAG could improve the fibrogenic and fibrolysis cascade via the regulation of excess activated and polarized KCs. SAG may also serve as a preventive and therapeutic agent in fibrosis of other organs for which current clinical therapy is unavailable.
机译：S-烯丙基 - 谷杆菌（SAG）是二烯丙基硫化物（DAS）的代谢物，大蒜的组分之一。 DAS表明了动物模型中对癌症的预防效果。但是，是否尚未研究合成缺陷是否可以改善肝纤维化。我们检查了慢性四氯化碳（CCU）给药对肝纤维化急性和慢性模型的潜在预防效果。 SAG抑制CCU诱导的肝纤维发生，以剂量依赖性方式和减少热休克蛋白-47（HSP47），胶原蛋白特异性伴侣和其他纤维化标志物。在纤维化回归模型中，在将CC1_4施用9周或二甲基亚甲胺（DMN）以进行6WK，在两种模型中明显加速纤维溶解。在DMN处理的肝脏的回归阶段，SAG标准化Kupffer细胞（KCS）中的M2表型（甘露糖受体表达）的比率。与这些结果一致，凹陷处理的M2-表型KC的培养上述剂抑制胶原-α1（I）链（COL1A1）mRNA表达在原代培养物活化的大鼠肝星状细胞（HSC）中。然而，下垂没有直接抑制HSC激活。在CC1_4单注射的急性模型中，凹陷抑制肝损伤剂量依赖于胆红素和ALT水平的抑制升高。这些发现表明，SAG通过调节过量活化和极化KCs可以改善纤维化和纤维分解级联。 SAG也可以作为预防性和治疗剂，其其他器官的纤维化是不可用的其他器官的纤维化。

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