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目的:探讨高血压大鼠心肌组织缝隙连接蛋白43(CX43)的表达,应用缬沙坦干预,研究其可能机制。方法:32只健康雄性SD大鼠随机分为空白对照组(n=8)、假手术组(n=8)以及模型组(n=16),模型组以二肾一夹方法建立,模型建立成功后,随机分为缬沙坦治疗组(n=8)和模型对照组(n=8)。治疗组给予缬沙坦按照30mg/(kg·d)剂量灌胃,空白对照组、假手术组以及模型对照组分别给予相同体积的生理盐水灌胃,每日一次。给药8周后,彩色多普勒超声检测心功能,麻醉处死动物,SP免疫组化法检测心肌组织中胰岛素样生长因子(IGF)-1、CX43及NF-κB的表达。结果:与空白对照组相比,假手术组IGF-1蛋白表达率、CX43及NF-κB表达变化不明显,心功能无明显变化,模型组则明显升高(P<0.05),心功能减弱(P<0.05);与模型对照组相比,缬沙坦治疗组上述指标则改善明显(P<0.05)。结论:肾血管性高血压大鼠心功能降低明显,与此同时IGF-1、CX43蛋白及NF-κB表达均显著增高,应用缬沙坦治疗8周后,上述指标均降低明显,同时心功能有明显改善,提示缬沙坦可通过降低IGF-1表达、抑制CX43表达改善心功能,NF-κB可能参与了这一过程。
AIM: To investigate the expression of connexin 43 (CX43) in myocardium of hypertensive rats and its possible mechanism by valsartan intervention. Methods: Thirty-two healthy male SD rats were randomly divided into blank control group (n = 8), sham operation group (n = 8) and model group (n = 16) After successful, the patients were randomly divided into valsartan treatment group (n = 8) and model control group (n = 8). The treatment group was given valsartan at a dose of 30mg / (kg · d), the control group, the sham operation group and the model control group were given the same volume of saline, once a day. After 8 weeks’ administration, the cardiac function was detected by color Doppler sonography, the animals were sacrificed by anesthesia, and the expression of insulin-like growth factor (IGF) -1, CX43 and NF-κB in myocardium were detected by SP immunohistochemistry. Results: Compared with the blank control group, the expression of IGF-1, CX43 and NF-κB in the sham-operated group had no significant changes, no significant changes in the cardiac function, and increased in the model group (P <0.05) (P <0.05). Compared with the model control group, the above indexes of valsartan treatment group improved obviously (P <0.05). CONCLUSION: The heart function of rats with renovascular hypertension is obviously decreased. At the same time, the expressions of IGF-1, CX43 and NF-κB are significantly increased. After 8 weeks of valsartan treatment, Valsartan could improve cardiac function by decreasing IGF-1 expression and inhibiting CX43 expression. NF-κB may be involved in this process.