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目的:研究忍冬木层孔菌醇提物抗肝纤维化的机制。方法:用2 m L/kg CCl4橄榄油溶液对大鼠腹腔注射制备肝纤维化模型。第1次注射后,给药组分别灌胃剂量相当于忍冬木层孔菌生药量1、0.5 g/kg的乙醇提取物,1次/d,共给药8 w。给药结束后,测定各组大鼠血清转化生长因子-β1(TGF-β1)、肝组织的总抗氧化能力(TAOC)、总超氧化物歧化酶(T-SOD)活性及丙二醛(MDA)含量;免疫组化测定α-平滑肌肌动蛋白(α-SMA)及基质金属蛋白酶-1(MMP-1)和基质金属蛋白酶抑制因子-1(TIMP-1)的表达。结果:与模型组比较,忍冬木层孔菌醇提物能降低模型大鼠血清中TGF-β1含量;升高肝组织T-SOD的活性及T-AOC水平,降低MDA含量;下调肝组织中α-SMA的表达,上调MMP-1的表达并下调TIMP-1的表达。结论:忍冬木层孔菌具有良好的抗氧化能力,具有防治肝纤维化的应用前景。其机制可能与抑制由氧化应激引发的肝星状细胞激活,并降低TGF-β1等激活肝星状细胞的细胞因子,上调促进胶原降解的MMP-1表达有关。
Objective: To study the mechanism of alcohol extract of Lonicera japonica against hepatic fibrosis. Methods: The model of hepatic fibrosis was induced by intraperitoneal injection of 2 m L / kg CCl4 olive oil solution. After the first injection, the rats in the treatment group were orally administered with ethanol extract at a dose of 1, 0.5 g / kg, which was administered once a day for 8 weeks. After the administration, the serum levels of TGF-β1, TAOC, T-SOD and malondialdehyde The content of MDA was measured. The expression of α-smooth muscle actin (α-SMA), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP- Results: Compared with the model group, the alcohol extract of Pseudomonas aeruginosa could decrease the content of TGF-β1 in the serum, increase the activity of T-SOD and the level of T-AOC in the liver, decrease the content of MDA, α-SMA, up-regulate the expression of MMP-1 and down-regulate the expression of TIMP-1. Conclusion: Pseudomonas aeruginosa has a good antioxidant capacity, with the application of prevention and treatment of hepatic fibrosis. The mechanism may be related to inhibition of hepatic stellate cell activation induced by oxidative stress and reduction of cytokines such as TGF-β1 and activation of hepatic stellate cells and up-regulation of the expression of MMP-1.