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表没食子儿茶素没食子酸酯对脂多糖诱导小鼠肝脏氧化应激、炎症和凋亡的影响

Effects of epigal ocatechin gal ate on oxidative stress, inflammation, and apoptosis in lipopolysaccharide-induced mouse liver

  • 摘要: 为探究表没食子儿茶素没食子酸酯(EGCG)对脂多糖(LPS)诱导的小鼠肝脏损伤的影响。将24只雄性BALB/c小鼠随机分为三组:Con组、LPS(腹腔注射10 mg·kg-1LPS)组和LPS+EGCG(灌胃80 mg·kg-1EGCG+腹腔注射10 mg·kg-1LPS)组。结果表明,与LPS攻毒组相比,灌胃EGCG小鼠的血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平显著降低;小鼠肝脏组织中抗氧化酶超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)水平显著升高,肝脏丙二醛(MDA)水平显著降低。同时,灌胃EGCG小鼠肝脏中促炎细胞因子肿瘤坏死因子(TNF)-α、白介素(IL)-1β、白介素(IL)-18和白介素(IL)-22的mRNA表达水平显著降低;肝脏中促凋亡相关蛋白Bax蛋白水平显著降低,抑制凋亡蛋白Bcl2和p-AMPK蛋白水平显著升高,Bcl2/Bax比值也显著升高。可知,EGCG可能通过激活AMPK途径抑制肝细胞凋亡,降低炎症因子表达,改善LPS诱导的小鼠肝脏病理损伤,缓解肝脏氧化应激。

     

    Abstract: To investigate the effect of epigallocatechin gallate(EGCG) on lipopolysaccharide(LPS)-induced liver injury in mice. Twenty-four male BALB/c mice were randomly divided into three groups: the Con group, LPS(intraperitoneal injection of 10 mg·kg-1LPS) group and LPS+EGCG(gavage 80 mg·kg-1EGCG+intraperitoneal injection of 10 mg·kg-1LPS) group. The results showed that compared with the LPS group, the serum alanine aminotransferase(ALT) and azelaic transaminase(AST) levels of the gavaged EGCG mice were significantly reduced; the levels of the antioxidant enzymes superoxide dismutase(SOD), catalase(CAT), and glutathione peroxidase(GSH-Px) in the liver tissues of the mice were significantly elevated, and the levels of malondialdehyde(MDA) in the livers of the mice were significantly reduced. Meanwhile, the m RNA expression levels of pro-inflammatory cytokines tumor necrosis factor(TNF)-α, interleukin(IL)-1β, interleukin(IL)-18 and interleukin(IL)-22 were significantly reduced in the livers of EGCG mice by gavage; the levels of pro-apoptosis-related protein Bax were significantly reduced in the livers, and the levels of inhibition of apoptosis proteins Bcl2 and p-AMPK were significantly elevated, and the Bcl2/Bax ratio was also significantly elevated. This suggested that EGCG might inhibit hepatocyte apoptosis and reduce the expression of inflammatory factors through activating the AMPK pathway, improve the pathological liver injury and alleviate the oxidative stress in the liver of LPS-induced mice.

     

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