| 全反式维甲酸对肝星状细胞活化及氧化应激的作用和机制探索 |
| 投稿时间：2023-12-21 修订日期：2024-05-09 点此下载全文 |
| 引用本文：修建平,杨朝爱,刘禧澳,潘乾禹,韦广旭,王卫星.全反式维甲酸对肝星状细胞活化及氧化应激的作用和机制探索[J].药学实践杂志,2024,42(7):291~296 |
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| 中文摘要:目的 探讨全反式维甲酸（ATRA）对肝星状细胞（HSCs）活化及氧化应激的作用和潜在机制。方法 应用10 ng/ml的血小板源性生长因子（PDGF-bb）诱导HSCs活化，以5 μmol/L剂量的ATRA处理48 h。检测细胞生长活力和表型标志物表达的变化，评价ATRA对HSCs活化的影响；检测细胞内活性氧（ROS）、还原型谷胱甘肽（GSH）和丙二醛（MDA）、抗氧化基因表达的变化，评价ATRA对HSCs氧化应激的影响；检测自噬标志物表达和自噬流的变化，评价ATRA对HSCs自噬活性的影响。结果 与PDGF-bb组相比，ATRA处理的HSCs生长活力显著降低（P<0.01），α-SMA和Collagen I蛋白的表达明显减少（P<0.01），细胞内ROS和MDA显著减少（P<0.01），GSH显著增加（P<0.01），抗氧化基因NRF2、HO-1和ATF4的表达明显增加（P<0.01）；同时自噬标志物Beclin 1和LC3 II/I的表达明显减少（P<0.01），自噬流信号显著降低。结论 ATRA显著抑制PDGF-bb诱导的HSCs活化，降低HSCs的氧化应激水平和自噬活性，对肝纤维化的防治具有潜在应用价值。 |
| 中文关键词:全反式维甲酸|肝星状细胞|激活|氧化应激|自噬 |
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| Exploration of the role and mechanism of all-trans retinoic acid on activation and oxidative stress of hepatic stellate cell |
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| Abstract:Objective To explore the role and potential mechanisms of all-trans retinoic acid （ATRA） on activation and oxidative stress of hepatic stellate cell （HSC）. Methods Platelet-derived growth factor （PDGF-bb, 10 ng/ml） was applied to induce the activation of HSCs, which was then treated with ATRA at a dosage of 5 μmol/L for 48 h. The effects of ATRA on HSC activation were evaluated by detecting changes in cell growth viability and phenotypic marker expression. The effects of ATRA on HSC oxidative stress were evaluated by detecting changes in intracellular reactive oxygen species （ROS）, reduced glutathione （GSH） and malondialdehyde （MDA）, and the expression of antioxidant genes. The effects of ATRA on HSC autophagic activity were evaluated by detecting changes in autophagy marker expression and autophagic flow. Results Compared with the PDGF-bb group, the cell viability was significantly reduced in ATRA-treated HSCs （P<0.01）, as well as the expression of α-SMA and Collagen I. The intracellular levels of ROS and MDA were significantly reduced in ATRA-treated HSCs （P<0.01）, whereas the GSH level was significantly increased （P<0.01）. The expression levels of antioxidant genes （NRF2, HO-1, and ATF4）, were significantly higher in ATRA-treated HSCs than those in the normal ones under PDGF-bb condition （P<0.01）. Meanwhile, the expression of autophagy markers Beclin 1 and LC3 Ⅱ/I, and signal of autophagy flow in ATRA-treated HSCs were found to be significantly reduced （P<0.01）. Conclusion ATRA significantly inhibited PDGF-bb-induced HSC activation and reduced the level of oxidative stress and autophagic activity of HSCs, which had potential applications in the prevention and treatment of liver fibrosis. |
| keywords:all-trans retinoic acid|hepatic stellate cells|activation|oxidative stress|autophagy |
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