目的 探究積雪草苷對(duì)代謝相關(guān)脂肪性肝病大鼠核因子E2相關(guān)因子2(Nrf2)、活性氧(ROS)通路表達(dá)的影響。方法 將大鼠隨機(jī)分為對(duì)照組、模型組、積雪草苷(5、15、30 mg/kg)組、雙環(huán)醇組,每組10只。除對(duì)照組外其余均建立脂肪肝模型,對(duì)照組與模型組給予ig 10 mL/kg生理鹽水,積雪草苷(5、15、30 mg/kg)組分別ig 5、15、30 mg/kg積雪草苷,雙環(huán)醇組ig 20 mg/kg雙環(huán)醇,1次/d,連續(xù)4周。采用ELISA檢測(cè)丙氨酸氨基轉(zhuǎn)移酶(ALT)、天冬氨酸氨基轉(zhuǎn)移酶(AST)水平及總膽固醇(TC)、三酰甘油(TG)含量,熒光探針-二氫乙啶(DHE)法檢測(cè)ROS水平,蘇木精-伊紅(HE)染色觀察病理組織,免疫印跡和PCR分別檢測(cè)Nrf1、Nrf2蛋白及mRNA相對(duì)表達(dá)量。結(jié)果 與模型組比較,積雪草苷15、30 mg/kg組ALT、AST、TC、TG、ROS水平顯著降低,Nrf1、Nrf2 mRNA及蛋白表達(dá)顯著升高(P<0.05),對(duì)照組大鼠肝臟組織結(jié)構(gòu)完好;積雪草苷15、30 mg/kg組及雙環(huán)醇組大鼠肝細(xì)胞脂肪變性有所減輕,匯管區(qū)見少量炎細(xì)胞浸潤(rùn)。結(jié)論 積雪草苷可降低代謝相關(guān)脂肪性肝病大鼠血清ALT、AST、TC、TG水平,并抑制ROS增長(zhǎng),其機(jī)制可能與激活Nrf1、Nrf2相關(guān)。

Objective To investigate the effects of asiaticoside on Nrf2 and ROS pathway expression in rats with metabolically associated fatty liver disease. Methods Rats were randomly divided into control group, model group, asiaticoside (5, 15, 30 mg/kg) group, and bicyclic alcohol group, with 10 rats in each group. Control group and model group were ig 10 mL/kg normal saline, asiaticoside (5, 15, 30 mg/kg) group were ig 5, 15, 30 mg/kg asiaticoside, bicyclic alcohol group were ig 20 mg/kg bicyclic alcohol group, once daily for 4 weeks. ELISA was used to detect ALT, AST, TC, and TG, fluorescent probe dihydroethidine (DHE) method was used to detect ROS, and HE staining was used to observe the pathological tissue. The relative expression levels of Nrf1 and Nrf2 protein and mRNA were detected by Western blotting and PCR respectively. Results Compared with model group, ALT, AST, TC, TG and ROS in 15 and 30 mg/kg asiaticoside groups were significantly decreased, while Nrf1 and Nrf2 mRNA and protein were significantly increased (P < 0.05). The liver structure of control group was intact. The hepatocyte steatosis of 15, 30 mg/kg asiaticoside group and dicyclol group was reduced, and a small amount of inflammatory cell infiltration was observed in the sink area. Conclusion Asiaticoside can reduce the levels of ALT, AST, TC, and TG in serum of rats with metabolism-related fatty liver disease, and inhibit the growth of ROS, which may be related to the activation of Nrf1 and Nrf2.

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