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汪辛强, 何飘, 朴美虹, 谢丽华, 曾阳, 王瑾茜, 张程程, 胡国恒, 陈亚.从肝治心组方对心肌缺血再灌注损伤大鼠心肌Nrf2、HO-1和铁转运相关蛋白的影响[J].湖南中医药大学学报,2025,45(1):23-29[点击复制] |
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| 从肝治心组方对心肌缺血再灌注损伤大鼠心肌Nrf2、HO-1和铁转运相关蛋白的影响 |
| 汪辛强,何飘,朴美虹,谢丽华,曾阳,王瑾茜,张程程,胡国恒,陈亚 |
| (湖南中医药大学第一附属医院, 湖南 长沙 410007;湖南中医药大学, 湖南 长沙 410208) |
| 摘要: |
| 目的 研究从肝治心组方对心肌缺血再灌注损伤（MIRI）大鼠心肌保护作用及核转录因子红系2相关因子2(Nrf2)、血红素加氧酶-1(HO-1)、二价金属转运蛋白1(DMT1)和膜铁转运辅助蛋白（Heph）表达的影响。方法 将60只SPF级雄性SD大鼠随机分为正常组、假手术组、模型组、从肝治心组方组[5.32 g/（kg·d）]、麝香保心丸组[10.27 mg/（kg·d）]、地尔硫艹卓组[6.86 mg/（kg·d）]，每组10只。通过结扎左前降支冠状动脉30 min后再灌注120 min，构建MIRI大鼠模型，术后连续灌胃给药14 d后取材。采用HE染色观察心肌组织形态学变化，普鲁士蓝染色观察心肌组织铁沉积情况，透射电子显微镜检测心肌组织超微结构，RT-PCR、Western blot检测Nrf2、HO-1、DMT1、Heph mRNA和蛋白表达情况。结果 与正常组和假手术组比较，模型组大鼠心肌纤维排列紊乱，纤维瘢痕组织增生，铁沉积水平高，线粒体结构异常，线粒体内脊模糊，Nrf2、HO-1、Heph mRNA和蛋白表达下调（P<0.05）,DMT1mRNA和蛋白表达上调（P<0.05）。与模型组比较，各给药组大鼠心肌组织病理损伤改善，铁沉积水平降低，线粒体和内脊结构较完整，Nrf2、HO-1、Heph mRNA和蛋白表达上调（P<0.05）,DMT1 mRNA和蛋白表达下调（P<0.05）。结论 从肝治心组方可能是通过激活Nrf2/HO-1信号通路，上调Heph的表达，下调DMT1的表达，减轻心肌组织铁沉积，发挥改善MIRI的作用。 |
| 关键词: 心肌缺血再灌注损伤 从肝治心组方 核因子E2相关因子2 血红素加氧酶-1 膜铁转运辅助蛋白 二价金属转运蛋白1 铁代谢失衡 |
| DOI：10.3969/j.issn.1674-070X.2025.01.004 |
| 投稿时间：2023-05-01 |
| 基金项目:全国名老中医药专家传承工作室建设项目(国中医药函人教函[2022]75号);湖南省自然科学基金项目(2021JJ40418);湖南省卫生健康委员会科研计划项目(202203074417);湖南中医药大学第一附属医院中医药传承创新专项(2024XYLH363);湖南中医药大学校级科研项目(Z2023XJYB25);湖南中医药大学中医学世界一流培育学科(2023)。 |
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| Effects of Conggan Zhixin Formula on Nrf2, HO-1, and iron transportrelated proteins in myocardial ischemia-reperfusion injury in rats |
| WANG Xinqiang, HE Piao, PO Meihong, XIE Lihua, CENG Yang, WANG Jinqian, ZHANG Chengcheng, HU Guoheng, CHEN Ya |
| (The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China;Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To study the myocardial protective effects of Conggan Zhixin Formula on myocardial ischemia-reperfusion injury（MIRI） in rats and its influence on the expressions of nuclear factor-erythroid 2-related factor 2（Nrf2）, heme oxygenase-1（HO-1）, divalent metal transporter 1（DMT1）, and hephaestin（Heph）. Methods Sixty male SPF-grade SD rats were randomly divided into normal group, sham-operated group, model group, Conggan Zhixin Formula group [5.32 g/（kg·d）], Shexiang Baoxin Pill group [10.27 mg/（kg·d）], and diltiazem group [6.86 mg/（kg·d）], with ten rats in each group. A MIRI rat model was established by ligating the left anterior descending coronary artery for 30 minutes followed by 120 minutes of reperfusion. Samples were collected after 14 consecutive days of gavage administration post-surgery. HE staining was used to observe the morphological changes in myocardial tissue, Prussian blue staining was employed to assess iron deposition in the myocardial tissue, and transmission electron microscopy was utilized to examine the ultrastructure of myocardial tissue. RT-PCR and Western blot were performed to examine the mRNA and protein expressions of Nrf2, HO-1, DMT1, and Heph. Results Compared with the normal group and sham-operated group, the model group exhibited disordered arrangement of myocardial fibers, fibrous scar tissue hyperplasia, high levels of iron deposition, abnormal mitochondrial structure with blurred cristae, and downregulated mRNA and protein expressions of Nrf2, HO-1, and Heph（P＜0.05）, as well as upregulated mRNA and protein expression of DMT1（P＜0.05）.Compared with the model group, the rats in each drug-administered group showed reduced morphological damage in the myocardial tissue, reduced levels of iron deposition, more intact mitochondrial and cristae structures, more intact mitochondrial and cristae structures, upregulated mRNA and protein expressions of Nrf2, HO-1, and Heph（P＜0.05）, and downregulated m RNA and protein expression of DMT1（P＜0.05）. Conclusion Conggan Zhixin Formula may exert its effects on reducing MIRI by activating the Nrf2/HO-1 signaling pathway, upregulating Heph expression, downregulating DMT1 expression, and reducing iron deposition in myocardial tissue. |
| Key words: myocardial ischemia-reperfusion injury Conggan Zhixin Formula nuclear factor-erythroid 2-related factor 2 heme oxygenase-1 membrane iron transporter accessory protein divalent metal transporter 1 iron metabolism imbalance |
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