ZHAO Tiantian,GUO Haidong,XUAN Shousong,et al.Effect of Electroacupuncture on Myocardial Inflammation, Chemokines and Cardiomyocyte Apoptosis in Mice with Acute Myocardial Infarction[J].zhongguo zhongyiyao xinxi zazhi,2021,28(1):44-48.[doi:10.19879/j.cnki.1005-5304.202008246]
电针对急性心肌梗死小鼠心肌组织炎症反应、趋化因子及心肌细胞凋亡水平的影响
- Title:
- Effect of Electroacupuncture on Myocardial Inflammation, Chemokines and Cardiomyocyte Apoptosis in Mice with Acute Myocardial Infarction
- 文章编号:
- 1005-5304(2021)01-0044-05
- Keywords:
- myocardial infarction; electroacupuncture; inflammation; chemokines; apoptosis ; mice
- 分类号:
- R245
- 文献标志码:
- A
- 摘要:
- 目的 观察电针对急性心肌梗死小鼠心肌组织炎症反应、趋化因子及心肌细胞凋亡水平的影响，探讨其保护心肌的作用机制。方法 结扎左冠状动脉前降支，构建小鼠急性心肌梗死模型。实验小鼠随机分为对照组、模型组和电针组，电针治疗3、7 d后，取心脏组织，分别用于制备冰冻切片和提取总RNA。免疫荧光染色检测梗死及周边区CD11b表达，RT-qPCR检测梗死及周边区炎症相关因子白细胞介素（IL）-10、IL-1β、肿瘤坏死因子-α（TNF-α）和趋化因子基质细胞衍生因子-1（SDF-1）、干细胞因子（SCF）及单核细胞趋化蛋白1（MCP-1）的表达，TUNEL染色检测梗死及周边区细胞凋亡情况。结果 与模型组比较，电针组梗死及周边区CD11b阳性表达下降（P＜0.05），促炎因子IL-1β相对表达量下调，治疗7 d时TNF-α明显上调（P＜0.01），IL-10、MCP-1无明显变化，SCF相对表达量治疗3 d时明显升高（P＜0.01）、SDF-1相对表达量治疗7 d时明显升高（P＜0.05），梗死及周边区心肌细胞凋亡明显减少（P＜0.05）。结论 电针可能通过抑制模型小鼠梗死区炎症反应，调节趋化因子水平，从而降低模型小鼠心肌损伤。
- Abstract:
- Objective To observe the effects of electroacupuncture (EA) on myocardial inflammation, chemokines and cardiomyocyte apoptosis in mice with acute myocardial infarction ( AMI); To explore the mechanism of its myocardial protection. Methods A mouse model of AMI was established by ligating the left anterior descending coronary artery. The mice were randomly divided into control group, model group and EA group. After the treatment of EA for 3 days and 7 days, heart tissues were harvested to prepare frozen sections, and total RNA was extracted. The expression of CD11b in the infarcted and surrounding areas was detected by immunofluorescence staining, and the inflammatory related factors IL-10, IL-1β, TNF-α, SCF, SDF-1 and chemokines MCP-1were detected t hrough RT-qPCR. The cell apoptosis in infarcted and surrounding area was detected by TUNEL staining. Results Compared with the model group, the positive expression of CD11b in the infarcted and surrounding area in the EA group decreased (P<0.05); the relative expression of pro-inflammatory factor IL-1β was down-regulated; TNF- α was significantly up-regulated after 7 days of treatment ( P<0.01); IL-10 and MCP-1 had no significant change; the relative expression of SCF of EA group was significantly increased after 3 days of treatment ( P<0.01); SDF-1 was significantly increased after 7 days of treatment (P<0.05); the apoptosis of myocardial cells in the infarcted and surrounding area of EA group was decreased (P<0.05). Conclusion EA may reduce myocardial injury in mice with AMI by inhibiting inflammationin infarcted area and regulating the expression of chemokines.
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备注/Memo
基金项目：国家自然科学基金（81704157、81673729）
更新日期/Last Update:
2020-12-18