基于温散法的肝积散对肝纤维化大鼠CTGF、TIMP-1、CB1、CB2的影响

Effects of Ganji Powder based on warming yang and expelling mass on the CTGF, TIMP-1, CB1 and CB2 of hepatic fi brosis rats

目的:观察基于温散法的肝积散对肝纤维化大鼠结缔组织生长因子(CTGF)、基质金属蛋白酶抑制剂(TIMP-1)、大麻素受体1(CB1)、CB2的影响,探讨其抗肝纤维化的作用机制。方法:Wistar雄性大鼠用40%的CCl4石蜡油腹腔注射造模,分为正常对照组、模型组、秋水仙碱片组、肝积散高、中、低剂量组。治疗8周后,检测各组大鼠肝组织中CTGF、TIMP-1、CB1、CB2的水平。结果:除肝积散低剂量组,各治疗组肝组织中CTGF表达明显低于模型组(P<0.05,P<0.01);肝积散中剂量组、秋水仙碱组肝组织中TIMP-1表达低于模型组(P<0.05);肝积散中、高剂量组、秋水仙碱组CB1表达明显低于模型组(P<0.05);肝积散低剂量组、秋水仙碱组CB2表达明显低于模型组(P<0.05,P<0.01)。结论:肝积散能够抑制细胞外基质(ECM)合成,促进其降解,抑制肝星状细胞(HSC)的增殖,阻止HSC的活化,这些可能是其抗肝纤维化的部分作用机制。

Objective： Through the experimental study of observing the effects of Ganji Powder based on wanning yang and expelling mass on the CTGF, TIMP-1, CB1 and CB2 of hepatic fibrosis rats, to explore its antihepatic fibrosis mechanism. Methods： Male Wistar rats model with hepatic fibrosis was induced by the intraperitoneal injection of 40% carbon tetrachloride paraffin oil. When hepatic fibrosis was verified to come into being by pathological examination, the rats were divided into normal control group, model group, colchicine tablets group, Ganji Powder high, medium, low dose groups. Uninterrupted treatment for 8 weeks, the CTGF, TIMP-1, CB1 and CB2 in liver tissues of all rats were examined. Results： In addition to Ganji Powder low dose group, CTGF expression in liver tissue of each treatment was significantly lower than that of model group group （P〈0.05, P〈0.01）. The expression of TIMP-1 in Ganji Powder medium dose group and colchicine tablets group was lower than that in the model group （P〈0.05）. The expression of CB1 in Ganji Powder medium and high dose group, colchicine group was significantly lower than that in the model group （P〈0.05）. The expression of CB2 in Ganji Powder low dose group, colchicine group was significantly lower than that in the model group （P〈0.05, P〈0.01）. Conclusion： Ganji Powder can inhibit the synthesis of ECM to promote its degradation, inhibit the proliferation of hepatic stellate cells, and prevent the activation of hepatic stellate cells. These may be a part of the mechanism of its anti-hepatic fibrosis action.