Electroacupuncture alleviates diabetic peripheral neuropathy through modulating mitochondrial biogenesis and suppressing oxidative stress.

IF 4.2 3区医学 Q1 ENDOCRINOLOGY & METABOLISM

World Journal of Diabetes Pub Date : 2025-02-15 DOI:10.4239/wjd.v16.i2.93130

Chong-Xi Yuan, Xuan Wang, Yun Liu, Tian-Cheng Xu, Zhi Yu, Bin Xu

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引用次数: 0

Abstract

Background: Peripheral neuropathy caused by diabetes is closely related to the vicious cycle of oxidative stress and mitochondrial dysfunction resulting from metabolic abnormalities. The effects mediated by the silent information regulator type 2 homolog-1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) axis present new opportunities for the treatment of type 2 diabetic peripheral neuropathy (T2DPN), potentially breaking this harmful cycle.

Aim: To validate the effectiveness of electroacupuncture (EA) in the treatment of T2DPN and investigate its potential mechanism based on the SIRT1/PGC-1α axis.

Methods: The effects of EA were evaluated through assessments of metabolic changes, morphological observations, and functional examinations of the sciatic nerve, along with measurements of inflammation and oxidative stress. Proteins related to the SIRT1/PGC-1α axis, involved in the regulation of mitochondrial biogenesis and antioxidative stress, were detected in the sciatic nerve using Western blotting to explain the underlying mechanism. A counterevidence group was created by injecting a SIRT1 inhibitor during EA intervention to support the hypothesis.

Results: In addition to diabetes-related metabolic changes, T2DPN rats showed significant reductions in pain threshold after 9 weeks, suggesting abnormal peripheral nerve function. EA treatment partially restored metabolic control and reduced nerve damage in T2DPN rats. The SIRT1/PGC-1α axis, which was downregulated in the model group, was upregulated by EA intervention. The endogenous antioxidant system related to the SIRT1/PGC-1α axis, previously inhibited in diabetic rats, was reactivated. A similar trend was observed in inflammatory markers. When SIRT1 was inhibited in diabetic rats, these beneficial effects were abolished.

Conclusion: EA can alleviate the symptoms of T2DNP in experimental rats, and its effects may be related to the mitochondrial biogenesis and endogenous antioxidant system mediated by the SIRT1/PGC-1α axis.

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电针通过调节线粒体生物发生和抑制氧化应激减轻糖尿病周围神经病变。

背景：糖尿病引起的周围神经病变与代谢异常引起的氧化应激和线粒体功能障碍的恶性循环密切相关。沉默信息调节因子2型同源物-1 (SIRT1)/过氧化物酶体增殖体激活受体- γ辅助激活因子-1α (PGC-1α)轴介导的作用为2型糖尿病周围神经病变（T2DPN）的治疗提供了新的机会，可能打破这种有害循环。目的：验证电针（EA）治疗T2DPN的有效性，并基于SIRT1/PGC-1α轴探讨其潜在机制。方法：通过代谢变化、形态学观察、坐骨神经功能检查以及炎症和氧化应激测量来评估EA的作用。利用Western blotting技术在坐骨神经中检测到SIRT1/PGC-1α轴相关蛋白，参与线粒体生物发生和抗氧化应激的调节，以解释其潜在机制。通过在EA干预期间注射SIRT1抑制剂来建立一个反证据组，以支持该假设。结果：T2DPN大鼠除糖尿病相关代谢改变外，9周后疼痛阈值明显降低，提示周围神经功能异常。EA治疗可部分恢复T2DPN大鼠的代谢控制，减轻神经损伤。模型组下调的SIRT1/PGC-1α轴在EA干预下上调。与SIRT1/PGC-1α轴相关的内源性抗氧化系统，先前在糖尿病大鼠中被抑制，被重新激活。在炎症标志物中也观察到类似的趋势。当SIRT1在糖尿病大鼠中被抑制时，这些有益作用就被消除了。结论：EA可减轻T2DNP实验大鼠的症状，其作用可能与SIRT1/PGC-1α轴介导的线粒体生物发生和内源性抗氧化系统有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

World Journal of Diabetes ENDOCRINOLOGY & METABOLISM-

自引率

2.40%

发文量

909

期刊介绍： The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.