基于JAK2/STAT3信号通路探究针刺治疗卒中后认知障碍的作用机制OA
Exploring the Mechanism of Acupuncture Treatment for Post-Stroke Cognitive Impairment Based on the JAK2/STAT3 Signaling Pathway
研究围绕针刺治疗卒中后认知障碍(PSCI)的作用机制展开,重点探讨了其对 JAK2/STAT3 信号通路的调控作用.PSCI 的发生发展与神经炎症、氧化应激及血脑屏障破坏密切相关,其中 JAK2/STAT3 信号通路的异常激活是关键的分子机制.研究表明,针刺通过多靶点、整体性调节作用,能有效下调关键促炎因子 IL-6 的水平,进而抑制 JAK2/STAT3 信号通路的过度活化.该通路的抑制减轻了神经炎症反应、缓解了氧化应激损伤、保护了血脑屏障完整性,最终促进了神经元修复与突触可塑性恢复.本综述为针刺治疗 PSCI 提供了科学的机制解释,也为开发针对 JAK2/STAT3 信号通路的 PSCI 治疗新策略提供了理论依据.未来研究需进一步明确针刺调控该通路的具体分子机制,并开展高质量的临床研究验证其疗效.
This study focuses on the mechanism of acupuncture treatment for post-stroke cognitive impairment(PSCI),with a particular emphasis on its regulatory effect on the JAK2/STAT3 signaling pathway.The occurrence and development of PSCI are closely related to neuroinflammation,oxidative stress and the disruption of the blood-brain barrier,among which the abnormal activation of the JAK2/STAT3 signaling pathway is the key molecular mechanism.Studies have shown that acupuncture,through multi-target and holistic regulatory effects,can effectively down-regulate the level of the key pro-inflammatory factor IL-6,thereby inhibiting the excessive activation of the JAK2/STAT3 signaling pathway.The inhibition of this pathway alleviated neuroinflammatory responses,alleviated oxidative stress damage,protected the integrity of the blood-brain barrier,and ultimately promoted neuronal repair and the recovery of synaptic plasticity.This review provides a scientific mechanism explanation for acupuncture treatment of PSCI and also offers a theoretical basis for the development of new strategies for PSCI treatment targeting the JAK2/STAT3 signaling pathway.Future research needs to further clarify the specific molecular mechanism by which acupuncture regulates this pathway and conduct high-quality clinical studies to verify its efficacy.
杨文雨;胡晓丽
辽宁中医药大学 辽宁 沈阳 110000辽宁中医药大学附属医院
JAK2/STAT3信号通路卒中后认知障碍机制
JAK2/STAT3 signaling pathwayPost-stroke cognitive impairmentMechanism
《中外医学研究》 2026 (8)
176-179,4
辽宁省科技计划联合计划(应用基础研究项目)(2023JH2/101700228)
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