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目的探讨姜黄素抗血吸虫病肝纤维化的作用及可能机制。方法小鼠随机分为4组:对照组、感染模型组、吡喹酮治疗组和姜黄素治疗组,除对照组外,各组建立血吸虫病肝纤维化小鼠动物模型,用实时荧光定量PCR反应观察小鼠肝组织过氧化物酶体增殖物激活受体γ(PPARγ)mRNA的表达。应用HE染色,免疫组化法及多媒体病理图文定量分析,观察各组小鼠肝脏的病理改变及转化生长因子β1(TGF-β1),α-平滑肌肌动蛋白(-αSMA)和Ⅰ、Ⅲ型胶原表达的变化。结果姜黄素可显著减轻肝脏纤维组织增生。感染模型组及吡喹酮治疗组PPARγmRNA表达较对照组及姜黄素治疗组显著减弱(P<0.05);姜黄素治疗组TGF-β1,-αSMA及Ⅰ、Ⅲ型胶原水平均明显低于吡喹酮治疗组和感染模型组(P<0.05)。结论姜黄素有明显的抗日本血吸虫病肝纤维化作用,其抗纤维化机制与其激活PPARγ的表达、抑制肝星状细胞(HSC)表达-αSMA及分泌TGF-β1,并减少Ⅰ、Ⅲ型胶原的合成有密切关系。
Objective To investigate the effect and possible mechanism of curcumin on hepatic fibrosis in schistosomiasis. Methods Mice were randomly divided into 4 groups: control group, infection model group, praziquantel treatment group, and curcumin treatment group. Except for the control group, each group was established an animal model of schistosomiasis liver fibrosis and real-time fluorescence quantitative PCR was used. The expression of peroxisome proliferator-activated receptor γ (PPARγ) mRNA in the liver of mice was observed. HE staining, immunohistochemistry, and multimedia pathology were used for quantitative analysis. The liver pathological changes and transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (-αSMA), and I and III were observed in each group. Changes in collagen expression. Results Curcumin can significantly reduce liver fibrosis. The expression of PPARγ mRNA in the model group and praziquantel treatment group was significantly lower than that in the control group and the curcumin group (P<0.05); the levels of TGF-β1, -αSMA, and type I and III collagen were significantly lower in the curcumin group than in the quinacridine group. Ketone treatment group and infection model group (P<0.05). Conclusion Curcumin has obvious anti-schistosomiasis effect on hepatic fibrosis, its anti-fibrotic mechanism and its activation of PPARγ expression, inhibition of hepatic stellate cells (HSC) expression -αSMA and secretion of TGF-β1, and reduce type I and III collagen The synthesis is closely related.