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埃他卡林对ET-1诱导的人肺动脉平滑肌细胞KATP通道蛋白表达的影响 被引量：1

Effects of Iptakalim on the expression of KATP protein in cultured human pulmonary artery smooth muscle cells induced by endothelin-1
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摘要 目的:研究新型ATP敏感性钾通道(KATP)开放剂埃他卡林对内皮素-1(ET-1)诱导的人肺动脉平滑肌细胞(HPASMCs)上KATP蛋白表达的影响。方法:原代培养人肺动脉平滑肌细胞,随机分成对照组,ET-1组,ET-1+埃他卡林组,ET-1+吡那地尔组,ET-1+埃他卡林+格列本脲组,ET-1+吡那地尔+格列本脲组,用Western-blot方法分析各组KATP蛋白磺酰脲受体亚单位(SUR2B)和内向整流性孔区亚单位(Kir6.1)表达变化情况。结果:与ET-1的作用相反,埃他卡林能使ET-1诱导下的SUR2B亚基表达升高,特异性KATP阻断剂格列本脲可逆转埃他卡林引起的SUR2B亚基表达升高;但各组对Kir6.1亚基表达无明显影响。结论:埃他卡林通过上调KATP的SUR2B亚基表达而发挥其在治疗低氧性肺动脉高压(HPH)中的作用,可望成为治疗低氧性肺动脉高压的新药。 Objective：To investigate the effects of Iptakalim, a novel ATP-sensitive potassium channel opener （KATPCO）,on the expression of ATP-sensitive potassium channel （KATP） protein in cultured human pulmonary artery smooth muscle cells（HPASMCs） induced by endothelin-I （ET-I）. Methods：By WesteIn-blot analysis,the expression of both SUR2B and Kir6.1 ,subunits of KATP protein, was detected in primary cultured HPASMCs, which were randomly divided into control group, ET-I group, ET-I ＋ Iptakalim group, ET-I＋ Pinacidil group,ET-l＋ Iptakalim＋ Glibenclamide group and ET-I ＋ Pinacidil＋ Glibenclamide group. Results：Compared with ET-1, Iptakalim could upregulate the SUR2B subunit expression,which could be inhibited by Glibenclamide,a particular ATP-sensitive potassium channel blocker. However, there was no significant difference in Kir6.1 subunit expression in each group. Conclusion： Iptakalim,a new potential candidate in the treatment of hypoxic pulmonary hypertension （HPH） ,could play an important role by upregulating the expression of SUR2B subunit.
作者 何志成 张石江 朱煜明 汤纳平 王虹 解卫平 倪布清 章斌
机构地区 南京医科大学第一附属医院胸心外科 南京医科大学第一附属医院呼吸内科 南京医科大学基础医学院药理学系
出处 《南京医科大学学报（自然科学版）》 CAS CSCD 北大核心 2008年第3期304-307,共4页 Journal of Nanjing Medical University(Natural Sciences)
基金 江苏省自然科学基金资助项目(BK2006246) 南京医科大学创新基金(CX2003002)
关键词 埃他卡林 低氧性肺动脉高压 WESTERN-BLOT ATP敏感性钾通道 ET-1 Iptakalim hypoxie pulmonary hypertension Western-blot ATP-sensitive potassium channel ET-1
分类号 Q786 [生物学—分子生物学]
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参考文献13

二级参考文献58

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共引文献29

同被引文献17

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南京医科大学学报（自然科学版）
2008年 第3期

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