槲皮素调控KCa3.1和NLRP3表达对大鼠PAH右心衰竭的保护作用

    Protective effects of quercetin regulating the expression of KCa3.1 and NLRP3 on PAH right heart failure in rats

    • 摘要:
      目的 测定大鼠心肌组织KCa3.1蛋白、NOD样受体热蛋白结构域相关蛋白3(NLRP3)蛋白,探讨槲皮素对缺氧性肺动脉高压(PAH)右心衰竭的保护作用。
      方法 选取清洁级雄性SD大鼠40只,分为正常对照组(Control组)、正常槲皮素组(CQ组)、缺氧组(H组)、缺氧槲皮素组(HQ组),每组10只。模型制备成功后,HE染色观察大鼠心肌纤维化情况;麦胚凝集素观察大鼠心肌细胞肥大水平;ELISA检测大鼠血清KCa3.1蛋白表达;Western blotting测定大鼠心肌组织KCa3.1蛋白、NLRP3蛋白表达;超声评估大鼠右心游离壁厚度;计算大鼠右心肥厚指数。
      结果 槲皮素可以降低PAH大鼠右心室肥厚指数,减轻右心室纤维化,并缓解右心室心肌细胞肥大(P < 0.01);Western blotting和ELISA结果显示槲皮素干预可以明显降低心肌KCa3.1和NLRP3的蛋白表达(P < 0.01)。
      结论 槲皮素对缺氧性PAH造成的右心衰竭有保护作用,可能与其抑制大鼠心肌KCa3.1与NLRP3表达有关。

       

      Abstract:
      Objective To detect the expression of KCa3.1 and NOD-like receptor heat protein domain associated protein 3(NLRP3) in rat myocardium, and investigate the protective effect of quercetin on hypoxic pulmonary artery hypertension(PAH) right heart failure.
      Methods Forty clean male SD rats were divided into the normal control group(Control group), normal quercetin group(group CQ), hypoxia group(group H) and hypoxia quercetin group(group HQ) (10 rats in each group).After the model was successfully prepared, the myocardial fibrosis of rats was observed by HE staining.The hypertrophy level of rat cardiomyocytes was observed by wheat germ lectin.The serum expression of KCa3.1 protein was detected by ELISA.The expression levels of KCa3.1 protein and NLRP3 in myocardial tissue were measured by Western blotting.The thickness of right heart free wall was evaluated by ultrasound.The right heart hypertrophy index of rats was calculated.
      Results Quercetin could decrease the right ventricular hypertrophy index, alleviate the right ventricular fibrosis, and relieve the right ventricular cardiomyocyte hypertrophy in PAH rats(P < 0.01).The results of Western blotting and ELISA showed that quercetin intervention could significantly inhibit the expression of myocardial KCa3.1 and NLRP3 proteins(P < 0.01).
      Conclusions Quercetin has a protective effect on right heart failure caused by hypoxic PAH, which may be related to its inhibition of KCa3.1 and NLRP3 expression in rat myocardium.

       

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