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目的:观察珠子参皂苷对四氯化碳(CCl4)致大鼠肝纤维化的保护作用及可能机制。方法:腹腔注射2ml/kg 50%CCl4橄榄油溶液制备大鼠肝纤维化模型,首次注射后分别灌胃给予珠子参皂苷(100和200mg/kg)和秋水仙碱(100 mg/kg),正常组和模型组给予等体积的0.5%羧甲基纤维素钠溶液,每天1次,共8周。8周后取血清,检测丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、总蛋白(TP)、白蛋白(ALB)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量;肝脏经组织匀浆和HE染色后,分析肝组织羟脯氨酸(Hyp)含量和形态学,计算肝纤维化分级、胶原纤维面积比、网状纤维面积比;实时定量PCR检测肝组织中SOD1、SOD2、SOD3、CAT和GPX1基因表达,Western blot检测细胞质和细胞核中Nrf2蛋白表达。结果:珠子参皂苷100和200mg/kg和秋水仙碱(100 mg/kg)能明显改善肝功能,降低血液中ALT、AST、ALP和MDA水平,增加SOD、GSH-Px、CAT活性和TP、ALB水平和A/G比值,降低肝纤维化分级、胶原纤维面积比、网状纤维面积比和Hyp含量,改善肝脏组织形态学;上调SOD1、SOD2、SOD3、CAT和GPX1基因表达和促进Nrf2核移位,增加肝细胞核内Nrf2的蛋白表达水平,特别是珠子参皂苷200mg/kg剂量组尤其显著。结论:珠子参皂苷对CCl4致大鼠肝纤维化具有较好的保护作用,促进Nrf2核移位和增强内源性抗氧化系统功能可能是其作用机制之一。
Objective: To observe the protective effect and the possible mechanism of Beoginseng saponins on liver fibrosis induced by carbon tetrachloride (CCl4) in rats. Methods: Rat model of hepatic fibrosis was induced by intraperitoneal injection of 2ml / kg 50% CCl4 olive oil solution. After the first injection, beads were given ginsenoside (100 and 200 mg / kg) and colchicine (100 mg / kg) Groups and model groups were given an equal volume of 0.5% sodium carboxymethyl cellulose solution once daily for 8 weeks. After 8 weeks, the serum was taken for detection of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total protein (TP), albumin (ALB) The activities of SOD, GSH-Px, CAT and the content of malondialdehyde (MDA) in the liver were measured. The liver tissues were homogenized and HE stained to analyze the liver Hyp contents and morphological changes of liver tissues were calculated, liver fibrosis grade, collagen fiber area ratio and reticular fiber area ratio were calculated. The expression of SOD1, SOD2, SOD3, CAT and GPX1 in liver tissue were detected by real-time quantitative PCR. blot was used to detect Nrf2 protein expression in cytoplasm and nucleus. Results: Bezins 100 and 200 mg / kg and colchicine (100 mg / kg) significantly improved liver function, decreased blood levels of ALT, AST, ALP and MDA, increased activities of SOD, GSH-Px and CAT, ALB level and A / G ratio decreased liver fibrosis grade, collagen fiber area ratio, reticular fiber area ratio and Hyp content, improve liver histomorphology; up-regulate SOD1, SOD2, SOD3, CAT and GPX1 gene expression and promote Nrf2 nuclear Shift, increase the level of Nrf2 protein in the nucleus of hepatocytes, especially the group of 200 mg / kg beads. CONCLUSION: Bezin can protect CCl4-induced hepatic fibrosis in rats, and it may be one of the mechanisms that Nrf2 nuclear translocation and enhancement of endogenous antioxidant system may be one of the mechanisms.