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作 者:唐诗慧 张丽[1] 方步武[1] TANG Shi-hui;Zhang Li;FANG Bu-wu(Depaament of Pharmacology,Tianjin Medical University,Tianjin 300070,China)
出 处:《天津医科大学学报》2018年第5期381-384,共4页Journal of Tianjin Medical University
摘 要:目的:研究蒿鳖养阴软坚方在体外对LX-2细胞的影响,从而探讨蒿鳖养阴软坚方对TGF-β1诱导的肝纤维化的作用。方法:体外培养人肝星状细胞LX-2,实验分为正常对照组、TGF-β1刺激组和蒿鳖养阴软坚方低、中、高浓度给药组。MTT法检测LX-2细胞增殖情况;比色法检测细胞培养液中乳酸脱氢酶(LDH)的活性;酶消化法检测细胞上清羟脯氨酸(Hyp)的含量;Western blot法检测collagenⅠ以及α-SMA蛋白表达量。结果:TGF-β1作用于LX-2能够明显促进细胞的增殖,collagen Ⅰ、α-SMA的表达量显著升高。蒿鳖养阴软坚方能抑制LX-2细胞增殖并且能够降低collagenⅠ和α-SMA的表达。结论:蒿鳖养阴软坚方能够显著抑制LX-2增殖,下调collagenⅠ和α-SMA的表达,降低Hyp生成,从而发挥抗肝纤维化的作用。Objective: To investigate the effect of HBYYRJ on hepatic stellate cells (HSCs, LX-2) in vitro, and explore the effect of HBYYRJ on liver fibrosis induced TGF-β1. Methods: LX-2 cells were cultured in vitro and divided into control group, TGF-β1 stimulation group and HBYYRJ low dose group, middle dose group and high dose group. The proliferation of LX-2 cells was detected by MTT assay; the activity of LDH was detected by colorimetric assay; and the content of Hyp was detected by enzyme digestion. Western blot was used to detect the protein expression of collagen Ι and α-SMA. Results: TGF-β1 significantly promoted the proliferation of LX-2, TGF-β1 significantly increased the level of collagen Ι and α-SMA. HBYYRJ significantly reduced the proliferation of LX-2, and significantly reduced the level of collagen Ι and α-SMA. Conclusion: HBYYRJ can significantly reduce the proliferation of LX-2, down-regulate the expression of collagen Ι and α-SMA, and decrease the synthesis of Hyp to attenuate hepatic fibrosis.
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