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作 者:梁晓强[1] 章学林[1] 顾宏刚[1] 张静喆[1]
机构地区:[1]上海中医药大学附属龙华医院,上海市宛平南路725号200032
出 处:《中医杂志》2017年第7期592-596,共5页Journal of Traditional Chinese Medicine
基 金:国家自然科学基金(81403305)
摘 要:目的探讨升清胶囊治疗胆石病的可能作用机制。方法选用人L-02肝细胞分为正常组,模型组,升清胶囊高、中、低剂量组及熊去氧胆酸高、中、低剂量组。除正常组外其余各组采用LXR激动剂诱导建立胆固醇沉积模型,各给药组每孔分别加入相应2 ml含10%药物血清,正常组和模型组每孔加入2 ml含10%空白血清进行培养。24 h后观察各组肝细胞上清液及细胞总胆固醇含量及肝细胞LXR-α、FXR、ABCA1、ABCG5及ABCG8 mRNA及蛋白表达。结果模型组上清液和肝细胞总胆固醇含量,LXR-α、FXR、ABCA1、ABCG5、ABCG8 mRNA蛋白较正常组均升高(P<0.01)。升清胶囊和熊去氧胆酸各剂量组总胆固醇含量及LXR-α、FXR、ABCA1、ABCG5、ABCG8 mRNA蛋白表达有不同程度的下降,其中升清胶囊和熊去氧胆酸片在降低LXR-α及ABCA1蛋白方面呈剂量依赖性,以高剂量组效果最好(P<0.05或P<0.01);并且在下调LXR-αmRNA表达方面,升清胶囊高剂量组效果优于熊去氧胆酸高剂量组(P<0.01)。结论升清胶囊可能通过降低LXR-α、FXR及其直接靶基因ABCA1、ABCG5、ABCG8 mRNA及蛋白表达,从而改善肝细胞内胆固醇沉积,抑制结石的形成和发展。Objective To explore the potential mechanism of Shengqing Capsule(升清胶囊,SC) in treating cholelithiasis. Methods Human L-02 hepatocytes were divided into normal group,model group and SC high,medium and low dose groups and ursodeoxycholic acid(UDCA) high,medium and low dose groups. The cholesterol deposition model was induced by liver X receptor(LXR) agonists in all groups except the normal group. Each treatment group was given 2ml serum containing 10% corresponding medicine for each hole,while the normal group and the model group were given 2ml blank serum for each hole. After 24 hours,volumes of total cholesterol(TC) in supernatant and cells in each group were observed,so were the mRNA and protein expressions of LXR-α,FXR,ABCA1,ABCG5 and ABCG8. Results In the model group,TC volume in both supernatant and cells,and the mRNA and protein expressions of LXR-α,FXR,ABCA1,ABCG5 and ABCG8 were all significantly higher than those in the normal group(P〈0. 01). While in each treatment group,they all decreased in varying degrees; in addition,SC and UDCA showed dose-dependence in decreasing LXR-α and ABCA1 proteins,with the best effect in high dose groups(P〈0. 05 or P〈0. 01). In downregulating LXR-α mRNA expression,the high dose SC group behaved significantly better than the high dose UDCA group(P〈0. 01). Conclusion By downregulating the mRNA and protein expressions of LXR-α and FXR,as well as their direct target gene ABCA1,ABCg4 and ABCG8,SC may ameliorate the cholesterol deposition in hepatocytes to inhibit the formation and development of calculi.
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