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电针刺激通过激活肥胖小鼠白色脂肪组织中的Y1受体诱导M1/M2极化,以减轻慢性炎症。

Electroacupuncture stimulation induced M1/M2 polarization in white adipose tissues by activating the Y1 receptor in obese mice to reduce chronic inflammation.

作者信息

Lu Mengjiang, Yu Ziwei, Yang Xingyu, Yang Ze, Xu Tiancheng, Yu Zhi, Jing Xinyue, An Li, Zhang Jianbin, Xu Bin

机构信息

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

School of Traditional Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, China.

出版信息

Adipocyte. 2025 Dec;14(1):2524638. doi: 10.1080/21623945.2025.2524638. Epub 2025 Jun 30.

Abstract

Chronic inflammation in obesity can induce complications such as diabetes and cardiovascular disease. Visceral adipose tissue is the main source of inflammation, but it is difficult to regulate effectively. Here, we investigated whether ES suppressed inflammation in eWAT and reduced chronic inflammation in obese individuals. We established a high-fat diet (HFD) model with C57BL/6J mice to measure chronic inflammation in obesity. In addition, the sympathetic nerve activity (SNA) was measured with the electrophysiological technique, the immunostaining and flow cytometry were used to detect the Y1 receptors in macrophage. Finally, the key role of the M1/M2 polarization in white adipose tissues by activating the Y1 receptor was verified by Y1 receptor antagonist BIBP3226. ES reduced the contents of IL-1β, TNF-α, IL-6 and TGF-β in the plasma and the mRNA expression of il-1 and tnfα in eWAT. Also, ES suppressed SNA in eWAT which regulated NPY1R receptor. In addition, ES induced M1/M2 polarization in eWAT via the Y1 receptor. The injection of a Y1 receptor (NPY1R) antagonist BIBP3226 restrained M1/M2 polarization. Further studies revealed that ES regulated sympathetic axons in eWAT to activate the Y1 receptor. This research demonstrates ES reduce chronic inflammation e mechanism is associated with the sympathetic Y1 receptor pathway, which promotes M1/M2 polarization.

摘要

肥胖中的慢性炎症会引发糖尿病和心血管疾病等并发症。内脏脂肪组织是炎症的主要来源,但难以有效调控。在此,我们研究了依替膦酸(ES)是否能抑制附睾白色脂肪组织(eWAT)中的炎症并减轻肥胖个体的慢性炎症。我们用C57BL/6J小鼠建立了高脂饮食(HFD)模型来测量肥胖中的慢性炎症。此外,采用电生理技术测量交感神经活动(SNA),用免疫染色和流式细胞术检测巨噬细胞中的Y1受体。最后,通过Y1受体拮抗剂BIBP3226验证了激活Y1受体在白色脂肪组织中M1/M2极化的关键作用。ES降低了血浆中白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和转化生长因子-β(TGF-β)的含量以及eWAT中il-1和tnfα的mRNA表达。此外,ES抑制了eWAT中调节神经肽Y1受体(NPY1R)的SNA。另外,ES通过Y1受体诱导eWAT中的M1/M2极化。注射Y1受体(NPY1R)拮抗剂BIBP3226可抑制M1/M2极化。进一步研究表明,ES调节eWAT中的交感神经轴突以激活Y1受体。本研究表明,ES减轻慢性炎症的机制与交感神经Y1受体途径有关,该途径促进M1/M2极化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7ec/12218457/6847fb70fcbd/KADI_A_2524638_F0001_OC.jpg

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