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目的观察柽柳乙醇提取物对小鼠酒精性肝损伤的保护作用,并对其分子机制进行初步探讨。方法采用慢性乙醇喂养加急性乙醇灌胃法诱导小鼠酒精性肝损伤。将80只雄性C57BL/6J小鼠随机分为5组:正常对照组、模型组、阳性对照组、柽柳低剂量组和柽柳高剂量组,每组16只。比较各组小鼠体质量、肝质量和肝指数之间的差别;通过HE染色和油红O染色观察肝组织的脂肪蓄积和损伤情况;检测外周血谷丙转氨酶(ALT)和甘油三酯(TG)以及肝脏中谷草转氨酶(AST)、超氧化物歧化酶(SOD)和丙二醛(MDA)水平;免疫组化法检测核苷酸结合寡聚化结构域样受体家族pyrin结构域蛋白3(NLRP3)炎性小体组成成份[NLRP3、凋亡相关微粒蛋白(ASC)、半胱氨酸蛋白酶-1(caspase-1)]和相关炎性因子IL-1β的蛋白表达水平。结果与模型组相比,柽柳高、低剂量组小鼠肝脏指数显著降低(P<0.05),肝脏脂肪蓄积和炎症情况明显减轻,血清中ALT和肝脏中AST水平显著降低(P<0.01);柽柳高剂量组肝脏MDA含量显著降低(P<0.05),SOD活性显著升高(P<0.05),肝脏中NLRP3、ASC、caspase-1和IL-1β的表达均显著减少(P<0.05)。结论柽柳可以在一定程度上抑制小鼠酒精性肝损伤的发生发展,其机制可能与抑制NLRP3-caspase-1-IL-1β通路活化有关。
Objective To observe the protective effect of ethanol extract from Tamarix oryzae on alcoholic liver injury in mice and to explore its molecular mechanism. Methods Alcohol-induced acute liver injury was induced by chronic ethanol feeding plus acute ethanol ingestion. Eighty male C57BL / 6J mice were randomly divided into five groups: normal control group, model group, positive control group, Tamarix chinensis low dose group and Tamarix chinensis high dose group, 16 rats in each group. The differences of body weight, liver mass and liver index of the mice in each group were compared; the accumulation and injury of liver tissue were observed by HE staining and oil red O staining; the levels of ALT and triglyceride TG, AST, SOD and MDA in the liver, and the pyrin domain of the nucleotide-binding oligomerization domain-like receptor family by immunohistochemistry (NLRP3), the expression of NLRP3, apoptosis associated protein (ASC), caspase-1 and the related inflammatory cytokines IL-1β. Results Compared with the model group, the liver index of Tamarix high and low dose groups was significantly decreased (P <0.05), the hepatic fat accumulation and inflammation were significantly reduced, and the levels of ALT and AST in serum were significantly decreased (P <0.01). The content of MDA in liver of Tamarix chinensis significantly decreased (P <0.05) and the activity of SOD was significantly increased (P <0.05). The expressions of NLRP3, ASC, caspase-1 and IL-1β in liver were significantly decreased (P <0.05). Conclusion Tamarix can inhibit the development of alcoholic liver injury in mice to a certain extent, the mechanism may be related to the inhibition of NLRP3-caspase-1-IL-1β pathway activation.