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神经-免疫相互作用在电针抗肥胖效应中的作用

Role of Neuro-Immune Cross-Talk in the Anti-obesity Effect of Electro-Acupuncture.

作者信息

Lu Mengjiang, He Yan, Gong Meirong, Li Qian, Tang Qianqian, Wang Xuan, Wang Yaling, Yuan Mengqian, Yu Zhi, Xu Bin

机构信息

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

The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.

出版信息

Front Neurosci. 2020 Feb 28;14:151. doi: 10.3389/fnins.2020.00151. eCollection 2020.

Abstract

There is evidence to show that electro-acupuncture (EA) has a promotive effect on both lipolysis and thermogenesis, and that these mechanisms underlie the anti-obesity effect of EA. The sympathetic nervous system (SNS) is known to play a role in thermogenesis. Additionally, obesity is characterized by a chronic low-grade inflammatory state. Based on these findings, the aim of the present study is to investigate the potential neuro-immune mechanisms underlying the therapeutic effect of EA in obesity. In the experiment, we used a high fat diet (HFD) rats model to study the effect of EA in reducing body weight. EA increases the activity of sympathetic nerves in inguinal white adipose tissue (iWAT), especially in the HFD group. Compared to HFD rats, EA can decrease sympathetic associated macrophage (SAM) and the level of norepinephrine transporter protein (Slc6a2). The relative uncoupling protein 1 expression shows EA increases thermogenesis in iWAT, and increases β3 receptors. Interestingly, injecting β antagonist in iWAT increases Slc6a2 protein levels. Additionally, the SNS-macrophage cross-talk response to EA showed in iWAT but not in epididymis white adipose tissue. The results of the present study indicate that EA exerts its anti-obesity effect via three mechanisms: (1) inhibition of SAMs and the norepinephrine transporter protein SlC6a2, (2) promoting SNS activity and thermogenesis, and (3) regulating immunologic balance.

摘要

有证据表明,电针(EA)对脂肪分解和产热均有促进作用,且这些机制是EA抗肥胖作用的基础。已知交感神经系统(SNS)在产热中起作用。此外,肥胖的特征是慢性低度炎症状态。基于这些发现,本研究的目的是探讨EA治疗肥胖症疗效的潜在神经免疫机制。在实验中,我们使用高脂饮食(HFD)大鼠模型来研究EA对体重减轻的影响。EA可增加腹股沟白色脂肪组织(iWAT)中交感神经的活性,尤其是在HFD组中。与HFD大鼠相比,EA可减少交感神经相关巨噬细胞(SAM)以及去甲肾上腺素转运蛋白(Slc6a2)的水平。相对解偶联蛋白1的表达表明EA可增加iWAT中的产热,并增加β3受体。有趣的是,在iWAT中注射β拮抗剂会增加Slc6a2蛋白水平。此外,SNS-巨噬细胞对EA的相互作用反应在iWAT中表现出来,但在附睾白色脂肪组织中未表现出来。本研究结果表明,EA通过三种机制发挥其抗肥胖作用:(1)抑制SAM和去甲肾上腺素转运蛋白SlC6a2;(2)促进SNS活性和产热;(3)调节免疫平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/926e/7059539/5d4469c5e0c6/fnins-14-00151-g001.jpg

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