Suppr超能文献

MFG-E8 通过调控整合素β3/ SOCS3/STAT3 通路改善小鼠神经损伤诱导的神经病理性疼痛

MFG-E8 Ameliorates Nerve Injury-Induced Neuropathic Pain by Regulating Microglial Polarization and Neuroinflammation via Integrin β3/SOCS3/STAT3 Pathway in Mice.

机构信息

Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.

出版信息

J Neuroimmune Pharmacol. 2024 Sep 21;19(1):49. doi: 10.1007/s11481-024-10150-w.

Abstract

Spinal microglial polarization plays a crucial role in the pathological processes of neuropathic pain following peripheral nerve injury. Accumulating evidence suggests that milk fat globule epidermal growth factor-8 (MFG-E8) exhibits anti-inflammatory effect and regulates microglial polarization through the integrin β3 receptor. However, the impact of MFG-E8 on microglial polarization in the context of neuropathic pain has not yet been investigated. In this study, we evaluated the effect of MFG-E8 on pain hypersensitivity and spinal microglial polarization following spared nerve injury (SNI) of the sciatic nerve in mice. We determined the molecular mechanisms underlying the effects of MFG-E8 on pain hypersensitivity and spinal microglial polarization using pain behavior assessment, western blot (WB) analysis, immunofluorescence (IF) staining, quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and small interfering RNA (siRNA) transfection. Our findings indicate that SNI significantly increased the levels of MFG-E8 and integrin β3 expressed in microglia within the spinal cord of mice. Additionally, we observed that intrathecal injection of recombinant human MFG-E8 (rhMFG-E8) alleviated SNI induced-mechanical allodynia and thermal hyperalgesia. Furthermore, the results suggested that rhMFG-E8 facilitated M2 microglial polarization and ameliorated neuroinflammation via integrin β3/SOCS3/STAT3 pathway in the spinal cord of mice with SNI. Importantly, these effects were negated by integrin β3 siRNA, or SOCS3 siRNA. These results demonstrate that MFG-E8 ameliorates peripheral nerve injury induced-mechanical allodynia and thermal hyperalgesia by driving M2 microglial polarization and mitigating neuroinflammation mediated by integrin β3/SOCS3/STAT3 pathway in the spinal cord of mice. MFG-E8 may serve as a promising target for the treatment of neuropathic pain.

摘要

脊髓小胶质细胞极化在周围神经损伤后神经病理性疼痛的病理过程中起着关键作用。越来越多的证据表明,牛奶脂肪球表皮生长因子 8(MFG-E8)通过整合素 β3 受体发挥抗炎作用并调节小胶质细胞极化。然而,MFG-E8 在外周神经损伤引起的神经病理性疼痛中的作用尚未得到研究。在这项研究中,我们评估了 MFG-E8 对 spared 神经损伤(SNI)后小鼠坐骨神经的神经病理性疼痛和脊髓小胶质细胞极化的影响。我们通过疼痛行为评估、Western blot(WB)分析、免疫荧光(IF)染色、定量聚合酶链反应(qPCR)、酶联免疫吸附测定(ELISA)和小干扰 RNA(siRNA)转染,确定了 MFG-E8 对疼痛过敏和脊髓小胶质细胞极化影响的分子机制。我们的研究结果表明,SNI 显著增加了小鼠脊髓中小胶质细胞中表达的 MFG-E8 和整合素 β3 的水平。此外,我们发现鞘内注射重组人 MFG-E8(rhMFG-E8)可缓解 SNI 诱导的机械性痛觉过敏和热痛觉过敏。此外,结果表明 rhMFG-E8 通过整合素 β3/SOCS3/STAT3 通路促进 M2 小胶质细胞极化并减轻 SNI 小鼠脊髓中的神经炎症。重要的是,这些作用被整合素 β3 siRNA 或 SOCS3 siRNA 所否定。这些结果表明,MFG-E8 通过驱动 M2 小胶质细胞极化并减轻整合素 β3/SOCS3/STAT3 通路介导的脊髓神经炎症,改善周围神经损伤引起的机械性痛觉过敏和热痛觉过敏。MFG-E8 可能成为治疗神经病理性疼痛的有前途的靶点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验