U-50488H抑制低氧诱导的原代肺动脉平滑肌细胞线粒体自噬

    U-50488H inhibits hypoxia-induced primary pulmonary artery smooth muscle cells mitophagy

      摘要
    • 摘要:
      目的 探讨低氧对肺动脉平滑肌细胞线粒体自噬的影响及κ-阿片受体激动剂U-50488H在其中的作用。
      方法 培养原代肺动脉平滑肌细胞，随机分组后进行低氧联合给药处理，检测线粒体自噬蛋白Bnip3及Pink1及其mRNA水平变化。
      结果 低氧处理1 d后，肺动脉平滑肌细胞Bnip3及Pink1蛋白水平显著上升(P<0.05)，U-50488H处理可以抑制Pink1的表达(P<0.01)；低氧联合自噬激动剂ABT-737处理后肺动脉平滑肌细胞线粒体自噬通路显著激活(P<0.01)，但可被U-50488H显著抑制(P<0.01)。
      结论 低氧处理1 d后肺动脉平滑肌细胞线粒体自噬水平显著升高，应用U-50488H后可以显著抑制低氧刺激导致的肺动脉平滑肌细胞线粒体自噬相关蛋白转录与翻译。

       

      Abstract:
      AIM To explored the effect of hypoxia on pulmonary artery smooth cells mitophagy, and the role of U-50488H, a kappa opioid receptor agonist, in this process.
      METHODS Primary pulmonary artery smooth muscle cells were cultured, and randomly grouped and treated with hypoxia and/or U-50488H, the mitophagy associated protein and mRNA level, such as Bnip3 and Pink1 were examined.
      RESULTS PASMCs Bnip3 and Pink1 level were significantly elevated after hypoxia for 24 h (P<0.05), U-50488H inhibited Pink1 expression (P<0.01), ABT-737, a mitophagy agonist combined hypoxia markedly elevated PASMCs mitophagy level (P<0.01), which was reversed when cells were treated with U-50488H (P<0.01).
      CONCLUSION PASMCs mitophagy level is noticeable elevated after 24 h hypoxia, κ-opioid receptor activation with U-50488Hinhibits mitophagy associated protein transcription and translation.

       

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