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观察不同低氧时段下,原代大鼠肺动脉平滑肌细胞(pulmonary arterial smooth muscle cells,PASMCs)ATP敏感性钾通道(ATP-sensitive potassium channel,K_(ATP)通道)蛋白的表达,探讨芪白平肺胶囊含药血清(简称QBPF)调控PASMCs K_(ATP)通道蛋白表达与一氧化氮(nitric oxide,NO)的相关性。清洁级SD大鼠给予芪白平肺胶囊颗粒连续灌胃10 d,制备芪白平肺含药血清。采用组织块贴壁法,体外培养原代大鼠肺动脉平滑肌细胞;Western blot检测不同低氧时间下Kir6.1和SUR2B的表达,以及在一氧化氮合酶抑制剂——Nω-硝基-L-精氨酸甲酯(Nω-nitro-L-arginine methyl ester,L-NAME)和K_(ATP)通道抑制剂——格列本脲(glyburide,GLYB)分别干预下,QBPF对其表达的影响。低氧6 h后Kir6.1和SUR2B蛋白表达开始上调,在低氧24 h达到高峰,低氧48,72 h的蛋白表达出现不同程度下调。在低氧24 h条件下,QBPF能进一步上调K_(ATP)通道Kir6.1和SUR2B蛋白表达,且这种上调作用能分别被K_(ATP)通道阻断剂GLYB和NO特异性阻断剂L-NAME所阻断,提示芪白平肺胶囊具有明确的K_(ATP)通道开放作用,其机制可能通过介导NO相关途径上调K_(ATP)通道蛋白表达,参与肺血管舒张作用,缓解COPD的发生发展。
To observe the expression of ATP-sensitive potassium channel (K-ATP) in primary rat pulmonary arterial smooth muscle cells (PASMCs) under different hypoxic periods, The capsule containing serum (QBPF) regulates the expression of K (ATP) channel protein and nitric oxide (NO) in PASMCs. Cleansing grade SD rats were given Qibai Pingfei capsule continuous gavage for 10 days to prepare Qibai Ping lung containing serum. The primary rat pulmonary artery smooth muscle cells were cultured in vitro using Western blot. The expression of Kir6.1 and SUR2B under different hypoxia time and the expression of NOS-N-nitro-L Effect of QBPF on Nω-nitro-L-arginine methyl ester (L-NAME) and K (ATP) channel inhibitor-glyburide (GLYB) . Kir6.1 and SUR2B protein expression began to increase after 6 h of hypoxia, peaked at 24 h of hypoxia, and down-regulated at 48 and 72 h of hypoxia. QBPF could up-regulate the expression of Kir6.1 and SUR2B in K (ATP) channels at 24 h of hypoxia, and this upregulation could be blocked by GLA-B and NO-specific blockers L -NAME, suggesting that Qibai Pingfei capsule has a clear K (ATP) channel opening effect, and its mechanism may be through the NO-related pathways upregulation of K (ATP) channel protein expression, involved in pulmonary vasodilation, relieve COPD Development took place.