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目的探讨缬沙坦对缺氧环境下肥大心肌细胞缝隙连接蛋白Cx43表达的影响。方法培养心肌细胞或在诱导肥大后分别缺氧24h,采用免疫荧光方法和Western-blot法分别检测缝隙连接蛋白Cx43总蛋白表达变化,同时观察缬沙坦对缺氧状态下肥大心肌细胞Cx43表达的影响。结果缺氧24h后可致正常心肌细胞Cx43表达下调13%(P<0.01),心肌细胞经血管紧张素Ⅱ诱导48h后可出现肥大,而肥大心肌细胞比正常心肌细胞在缺氧24h后Cx43总蛋白表达显示出更明显的下调(P<0.01),缬沙坦可抑制缺氧状态下肥大心肌细胞的凋亡和Cx43总蛋白表达的下调。结论缺氧可导致心肌细胞Cx43表达下调,而肥大心肌细胞在缺氧时总蛋白下调更为明显,而缬沙坦可部分抑制肥大心肌细胞缺氧时的凋亡和Cx43总蛋白下调,这可能与缬沙坦改善缺氧时肥大心肌的电生理重构和恶性心律失常的机制有关。
Objective To investigate the effects of valsartan on the expression of connexin Cx43 in hypertrophic cardiomyocytes under hypoxia. Methods Cardiomyocytes were cultured or hypoxia was induced after hypertrophy for 24 h. Immunofluorescence and Western-blot were used to detect the expression of Cx43 protein. The effects of valsartan on the expression of Cx43 in hypertrophic cardiomyocytes influences. Results After hypoxia for 24 hours, the expression of Cx43 in normal cardiomyocytes was down-regulated by 13% (P <0.01), and the hypertrophy of hypertrophic cardiomyocytes induced by angiotensin Ⅱ was observed in 24 h after hypoxia compared with that in normal cardiomyocytes (P <0.01). Valsartan can inhibit the apoptosis of hypertrophic cardiomyocytes and the downregulation of total Cx43 protein in hypoxia. Conclusions Hypoxia can lead to the down-regulation of Cx43 expression in cardiomyocytes, whereas hypertrophic cardiomyocytes down-regulated the expression of total protein in hypoxia more obviously, while valsartan could partially inhibit the apoptosis and down-regulation of Cx43 total protein in hypertrophic cardiomyocytes during hypoxia. And valsartan to improve hypoxia myocardial hypertrophy electrophysiological remodeling and malignant arrhythmia mechanism.