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目的:观察姜黄素对非酒精性脂肪性肝病(NAFLD)大鼠肝脏组织PGC1α基因的去甲基化作用。方法:21只SD雄性大鼠随机分3组(每组n=7),干预组首先以高脂饲料喂养8周(建立NAFLD大鼠模型),然后加用姜黄素灌胃4周;NAFLD组以高脂饲料喂养8周后加用姜黄素模拟物灌胃4周;正常组始终常规喂养12周。采用全自动生化分析仪检测各组大鼠血清他、TC、AST、ALT及肝组织TG、TC:焦磷酸测序法检测大鼠肝组织PGC1α基因启动子区-260位点的甲基化水平:RT-PCR检测肝组织PGC1αmRNA水平。结果:(1)NAFLD组外周血TG、TC、AST、ALT及肝细胞TG、TC比正常组显著升高(P<0.05),干预组以上参数较NAFLD组显著下降(P<0.05);(2)NAFLD组PGC1α启动子区CpG甲基化率显著高于正常组(P<0.01),干预组甲基化率较NAFLD组显著下降(P<0.01):(3)NAFLD组肝脏组织PGC1αmRNA的表达量比正常组显著下降(P<0,01),干预组PGC1αmRNA的表达量较NAFLD组显著升高(P<0.01)。结论:姜黄素通过对肝脏PGC1α启动子区有去甲基化作用改善大鼠肝脏脂肪变性。
Objective: To observe the demethylation of curcumin on PGC1α gene in liver of non-alcoholic fatty liver disease (NAFLD) rats. Methods: Twenty-one male Sprague-Dawley rats were randomly divided into three groups (n = 7 each). The intervention group was fed with high-fat diet for 8 weeks (NAFLD-induced rat model) and then with curcumin for 4 weeks. NAFLD group After 8 weeks of feeding with high-fat diet, curcumin mimic plus gavage was given for 4 weeks. Normal group was fed with normal diet for 12 weeks. TC, AST, ALT and liver tissue TG, TC: Pyrosequencing were used to detect the methylation level of PGC1α gene promoter-260 in rat liver tissue by automatic biochemistry analyzer: RT-PCR detection of liver tissue PGC1α mRNA levels. Results: (1) TG, TC, AST, ALT, TG and TC in peripheral blood of NAFLD group were significantly higher than those in normal group (P <0.05), and the above parameters in intervention group were significantly lower than those in NAFLD group (P <0.05) 2) The CpG methylation rate of PGC1α promoter in NAFLD group was significantly higher than that in normal group (P <0.01), and the methylation rate of PGF1α in NAFLD group was significantly lower than that in NAFLD group (P <0.01). (3) The expression of PGC1α mRNA in the intervention group was significantly higher than that in the NAFLD group (P <0.01). Conclusion: Curcumin can improve hepatic steatosis in rats through demethylation of PGC1α promoter in liver.