[1]刘希鹏,张美芳,张海峰,等.PPAR-γ调控的自噬通路在染料木黄酮抑制肝星状细胞激活过程中的作用[J].南方医科大学学报,2019,(05):561.[doi:10.12122/j.issn.1673-4254.2019.05.10]
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PPAR-γ调控的自噬通路在染料木黄酮抑制肝星状细胞激活过程中的作用()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2019年05期
页码:
561
栏目:
出版日期:
2019-05-15

文章信息/Info

Title:
Role of PPAR-γ-regulated autophagy in genistein-induced inhibition of hepatic stellate cell activation
作者:
刘希鹏张美芳张海峰赵安达孙娟唐雯
关键词:
染料木黄酮肝星状细胞自噬PPAR-γ
Keywords:
genistein hepatic stellate cells autophagy PPAR-γ
DOI:
10.12122/j.issn.1673-4254.2019.05.10
摘要:
目的探讨染料木黄酮在体外抑制肝星状细胞(HSC)活化的效应以及PPAR-γ调控的自噬通路在其中发挥的作用。方法 将体外培养的HSC细胞分别给予不同浓度的染料木黄酮作用48 h后,用Western blot法测定HSC激活标志蛋白α-SMA、α1(I) collagen的表达以及自噬相关蛋白LC3Ⅱ\p62和PPAR-γ的表达;利用自噬抑制剂和PPAR-γ抑制剂验证自噬在染料木黄酮抑制 HSC激活过程中的作用以及PPAR-γ对自噬的调控作用。结果染料木黄酮作用于HSC细胞后,HSC活化标志蛋白α-SMA、α1 (I)collagen的水平明显降低(P<0.05),而自噬相关蛋白LC3Ⅱ的表达明显升高、泛素结合蛋白p62水平明显降低,同时PPAR-γ 表达明显增加(P<0.05);与单纯染料木黄酮刺激组相比,用3-MA处理后HSC活化标志蛋白α-SMA、α1(I)collagen的表达明显 升高;并且加入PPAR-γ抑制剂后,自噬相关蛋白LC3Ⅱ的表达明显降低、泛素结合蛋白p62 水平明显增加(P<0.05)。结论 PPAR-γ调控的自噬通路在染料木黄酮抑制HSC细胞激活的过程中发挥着重要作用。
Abstract:
Objective To investigate the inhibitory effect of genistein on activation of hepatic stellate cells (HSCs) in vitro and the role of the autophagy pathway regulated by PPAR-γ in mediating this effect. Methods Cultured HSC-T6 cells were exposed to different concentrations of genistein for 48 h, and HSC activation was verified by detecting the expressions of α-SMA and α1(I) collagen; autophagy activation in the cells was determined by detecting the expressions of LC3-II and p62 using Western blotting. The autophagy inhibitor 3-MA was used to confirm the role of autophagy in genistein- induced inhibition of HSC activation. A PPAR-γ inhibitor was used to explore the role of PPAR-γ in activating autophagy in the HSCs. Results Genistein at concentrations of 5 and 50 μmol/L significantly inhibited the expressions of α-SMA and α1(I) collagen (P<0.05), markedly upregulated the expressions of PPAR-γ and the autophagy-related protein LC3-II (P<0.05) and significantly down-regulated the expression of the ubiqutin-binding protein p62 (P<0.05) in HSC-T6 cells. The cells pretreated with 3-MA prior to genistein treatment showed significantly increased protein expressions of α-SMA and α1(I) collagen compared with the cells treated with genistein only (P<0.05). Treatment with the PPAR-γ inhibitor obviously lowered the expression of LC3-II and enhanced the expression p62 in genistein-treated HSC-T6 cells, suggesting the activation of the autophagy pathway. Conclusion PPAR-γ- regulated autophagy plays an important role in mediating genistein-induced inhibition of HSC activation in vitro.

相似文献/References:

[1]张玉坤,王导新,朱涛,等.染料木黄酮通过上调血红素氧合酶-1表达减缓野百合碱诱导的大鼠肺动脉高压[J].南方医科大学学报,2012,(02):151.
[2]史海涛,董蕾,刘亚萍,等.高糖环境对肝星状细胞TLR4表达及脂多糖诱导的炎症因子表达的影响[J].南方医科大学学报,2013,(03):386.
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更新日期/Last Update: 1900-01-01