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电针对心肌缺血小鼠模型通过调节心脏自主重构改善心功能和减小梗死面积。

Electroacupuncture improves cardiac function and reduces infarct size by modulating cardiac autonomic remodeling in a mouse model of myocardial ischemia.

机构信息

Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, China.

Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

出版信息

Acupunct Med. 2021 Dec;39(6):681-690. doi: 10.1177/09645284211009536. Epub 2021 May 30.

Abstract

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.

摘要

背景

交感神经和副交感神经重塑在心肌缺血(MI)损伤后的心脏功能中起着重要作用。越来越多的证据表明,电针(EA)通过调节自主神经系统(ANS)来调节心脏功能,但对于其在 MI 后神经重塑方面的效果知之甚少。

目的

研究 EA 在 MI 后 ANS 重塑中的作用。

方法

雄性 C57/BL6 成年小鼠通过结扎左前降支(LAD)冠状动脉成功建立 MI 模型后,平均分为对照组(Ctrl)、MI 组和 EA 组。在进行连续 5 天的 EA 治疗后,通过超声心动图和 2,3,5-三苯基四氮唑(TTC)染色评估心脏功能和梗死面积。通过 ELISA 测量血清去甲肾上腺素(NE)水平来定量交感神经激活。然后,通过免疫组织化学(IHC)、RT-qPCR 和 Western blot 检测 ANS 重塑。

结果

我们的初步研究结果表明,EA 可增加 MI 损伤后的心搏出量和射血分数,并减少梗死面积。与 MI 组相比,EA 组血清 NE 水平显著降低。IHC 染色结果表明,EA 组生长相关蛋白(GAP)43 和酪氨酸羟化酶(TH)阳性神经纤维的密度降低,而胆碱乙酰转移酶(CHAT)和囊泡乙酰胆碱转运体(VACHT)增加。同时,结果证实,EA 治疗可显著抑制 MI 小鼠 GAP43 和 TH 的 mRNA 和蛋白表达,同时伴有 CHAT 和 VACHT 的升高。

结论

EA 治疗可通过调节 MI 后交感神经和副交感神经重塑来改善心脏功能和减少梗死面积,从而帮助心脏 ANS 达到新的平衡,试图保护心脏免受进一步可能的损伤。

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