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黄静静1,陈浩2,黄希1▲.基于Nrf2/ARE信号通路探讨宽胸气雾剂对血瘀型大鼠心脏的保护及机制[J].中国医药科学,2024,14(9):18-21        基金项目:福建中医药大学校管临床专项(XB2021040)
基于Nrf2/ARE信号通路探讨宽胸气雾剂对血瘀型大鼠心脏的保护及机制
Exploring the protection and mechanism of broad chest aerosol on the heart of blood stasis type rats based on the Nrf2/ARE signal pathway
  
DOI:
中文关键词:  心肌缺血再灌注损伤;Nrf2/ARE信号通路;宽胸气雾剂;血瘀证
英文关键词:Myocardial ischemia reperfusion injury; Nrf2/ARE signaling pathway; Kuanxiong Aerosol; Blood stasis
作者单位
黄静静1,陈浩2,黄希1▲ 1.福建中医药大学附属第三人民医院心血管科,福建福州 350108; 2.解放军联勤保障部队第九〇〇医院心血管科,福建福州 350001 
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中文摘要:
      [摘要] 目的 探讨宽胸气雾剂(KA)对大鼠心肌缺血再灌注损伤(MIRI)的保护作用及其可能机制。 方法 随机将30只健康的SD雄性大鼠分为假手术(SHAM)组、MIRI组、MIRI+KA组,给药(生理盐水)28 d后构建MIRI模型,采用结扎冠状动脉方法建立小鼠MIRI模型,术后继续对MIRI+KA组进行KA干预,每次1揿,每日2次。SHAM组和MIRI组给予生理盐水,每日1次。术后收集小鼠心肌组织,称取小鼠心脏重量,HE染色观察组织病理学改变,免疫印迹法检测氧化应激和细胞凋亡相关蛋白表达。 结果 MIRI组小鼠心肌间质出现明显的炎症细胞浸润,促氧化应激蛋白MDA表达升高,SOD、CAT蛋白表达降低(P < 0.05)。KA处理可使MIRI诱导的小鼠心脏重量和心脏重量指数明显降低,心肌间质炎症细胞浸润减少,SOD蛋白表达改善。此外,KA处理还能显著增加转录因子NR-F-相关因子2(Nrf2)蛋白表达,降低抗氧化反应元件(ARE)蛋白表达(P < 0.05)。 结论 KA可以改善血瘀型大鼠的MIRI,其心肌保护机制可能与Nrf2/ARE信号通路有关。
英文摘要:
      [Abstract] Objective To elucidate the protective effect and possible mechanism of Kuanxiong Aerosol (KA) on myocardial ischemia reperfusion injury (MIRI) in rats. Methods Thirty healthy male rats were randomly divided into a sham surgery group (SHAM) group, a MIRI group, and a MIRI+KA group. After 28 days of administration (physiological saline), a MIRI model was constructed, and a mouse MIRI model was established by ligating the coronary artery. After surgery, the MIRI+KA group continued to receive KA intervention, with one press each time and twice a day. The SHAM group and MIRI groups were given physiological saline once a day. Collect mouse myocardial tissue after surgery and weigh the mouse heart. HE staining was used to observe histopathological changes in the tissue; Western blot was used to detect the expression of oxidative stress and apoptosis related proteins. Results The MIRI group mice showed significant infiltration of inflammatory cells in the myocardial interstitium, increased expression of oxidative stress protein MDA, and decreased expression of SOD and CAT proteins (P < 0.05). The treatment with KA can significantly reduce the heart weight and heart weight index induced by MIRI in mice, reduce the infiltration of inflammatory cells in the myocardial interstitium, and improve the expression of SOD protein. In addition, treatment with KA can significantly increase the expression of nuclear factor erythroid-2 related factor 2 (Nrf2) protein and reduce the expression of antioxident response element (ARE) protein (P < 0.05). Conclusion KA has protective effect on myocardial ischemia-reperfusion injury in mice, and its protective mechanism may be related to the activation of Nrf2/ARE signaling pathway.
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