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

IF 3.1 4区 生物学 Q2 ENDOCRINOLOGY & METABOLISM
Adipocyte Pub Date : 2025-12-01 Epub Date: 2025-06-30 DOI:10.1080/21623945.2025.2524638
Mengjiang Lu, Ziwei Yu, Xingyu Yang, Ze Yang, Tiancheng Xu, Zhi Yu, Xinyue Jing, Li An, Jianbin Zhang, Bin Xu
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引用次数: 0

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.

电针刺激通过激活肥胖小鼠Y1受体,诱导白色脂肪组织M1/M2极化,减轻慢性炎症。
肥胖引起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,但很难有效调节。在这里,我们研究ES是否抑制eWAT的炎症并减少肥胖个体的慢性炎症。我们用C57BL/6J小鼠建立高脂饮食(HFD)模型,测量肥胖的慢性炎症。采用电生理技术检测大鼠交感神经活动(SNA),免疫染色和流式细胞术检测巨噬细胞中Y1受体的表达。最后,通过Y1受体拮抗剂BIBP3226验证了M1/M2极化通过激活Y1受体在白色脂肪组织中的关键作用。ES降低了血浆中il-1 β、TNF-α、IL-6和TGF-β的含量以及eWAT中il-1和TNF-α的mRNA表达。此外,ES还抑制了eWAT中的SNA,从而调控了NPY1R受体。此外,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抑制M1/M2极化。进一步的研究表明,ES调节eWAT的交感轴突激活Y1受体。本研究表明ES减轻慢性炎症的机制与交感Y1受体通路有关,该通路促进M1/M2极化。
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来源期刊
Adipocyte
Adipocyte Medicine-Histology
CiteScore
6.50
自引率
3.00%
发文量
46
审稿时长
32 weeks
期刊介绍: Adipocyte recognizes that the adipose tissue is the largest endocrine organ in the body, and explores the link between dysfunctional adipose tissue and the growing number of chronic diseases including diabetes, hypertension, cardiovascular disease and cancer. Historically, the primary function of the adipose tissue was limited to energy storage and thermoregulation. However, a plethora of research over the past 3 decades has recognized the dynamic role of the adipose tissue and its contribution to a variety of physiological processes including reproduction, angiogenesis, apoptosis, inflammation, blood pressure, coagulation, fibrinolysis, immunity and general metabolic homeostasis. The field of Adipose Tissue research has grown tremendously, and Adipocyte is the first international peer-reviewed journal of its kind providing a multi-disciplinary forum for research focusing exclusively on all aspects of adipose tissue physiology and pathophysiology. Adipocyte accepts high-profile submissions in basic, translational and clinical research.
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