在心肌缺血小鼠模型中,电针通过调节心脏自主神经重构改善心功能并减少梗死面积。

Sheng-Feng Lu, Jun-Meng Wang, Jing Yuan, Wen-Xiu Yang, Li-Yao Chen, Tao Zhang, Xin-Yue Jing, Yi Zhuang, Cheng-Shun Zhang, Shu-Ping Fu, Mei-Ling Yu
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引用次数: 6

摘要

背景:交感神经和副交感神经重构在心肌缺血(MI)损伤后的心功能中起重要作用。越来越多的证据表明,电针(EA)可以通过调节自主神经系统(ANS)来调节心功能,但其对心肌梗死后神经重构的有效性知之甚少。目的:探讨EA在心肌梗死后ANS重构中的作用。方法:将成年雄性C57/BL6小鼠结扎左前降支(LAD)制成心肌梗死模型,随机分为对照组(Ctrl)、心肌梗死组和EA组。采用超声心动图和2,3,5-三苯四唑(TTC)染色评价EA连续5天后的心功能和梗死面积。ELISA法测定血清去甲肾上腺素(NE)水平,定量交感神经激活。然后采用免疫组化(IHC)、RT-qPCR和Western blotting检测ANS重构。结果:我们的初步研究结果表明,EA增加了心肌梗死后的射血分数和分数缩短,减少了梗死面积。与心肌梗死组相比,EA组血清NE水平显著降低。免疫组化染色结果显示,EA组生长相关蛋白(GAP)43和酪氨酸羟化酶(TH)阳性神经纤维密度降低,胆碱乙酰转移酶(CHAT)和囊泡乙酰胆碱转运蛋白(VACHT)升高。同时,结果证实,EA处理显著抑制心肌梗死小鼠GAP43和TH mRNA和蛋白表达,并伴有CHAT和VACHT升高。结论:EA治疗可通过调节心肌梗死后交感和副交感神经重构,改善心功能,缩小梗死面积,使心肌ANS达到新的平衡,保护心脏免受进一步损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture improves cardiac function and reduces infarct size by modulating cardiac autonomic remodeling in a mouse model of myocardial ischemia.

Background: Sympathetic and parasympathetic nerve remodeling play an important role in cardiac function after myocardial ischemia (MI) injury. Increasing evidence indicates that electroacupuncture (EA) can regulate cardiac function by modulating the autonomic nervous system (ANS), but little is known about its effectiveness on neural remodeling post-MI.

Objectives: To investigate the role of EA in ANS remodeling post-MI.

Methods: Adult male C57/BL6 mice were equally divided into the Control (Ctrl), MI and EA groups after generating the MI model by ligating the left anterior descending (LAD) coronary artery. Echocardiography and 2,3,5-triphenyltetrazolium (TTC) staining were employed to evaluate cardiac function and infarct size after EA treatment for five consecutive days. Serum norepinephrine (NE) levels were measured by ELISA to quantify sympathetic activation. Then, ANS remodeling was detected by immunohistochemistry (IHC), RT-qPCR, and Western blotting.

Results: Our preliminary findings showed that EA increased ejection fraction and fractional shortening and reduced infarct area after MI injury. Serum NE levels in the EA group were significantly decreased compared with those in the MI group. IHC staining results demonstrated that the density of growth associated protein (GAP)43 and tyrosine hydroxylase (TH) positive nerve fibers in the EA group were decreased with increased choline acetyltransferase (CHAT) and vesicular acetylcholine transporter (VACHT). Meanwhile, the results verified that mRNA and protein expression of GAP43 and TH were significantly inhibited by EA treatment in the MI mice, accompanied by elevated CHAT and VACHT.

Conclusions: EA treatment could improve cardiac function and reduce infarct size by modulating sympathetic and parasympathetic nerve remodeling post-MI, thus helping the cardiac ANS reach a new balance to try to protect the heart from further possible injury.

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