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葡萄籽原花青素通过调节脊髓损伤大鼠小胶质细胞 M1/M2 极化发挥神经保护作用。

Grape Seed Proanthocyanidins Exert a Neuroprotective Effect by Regulating Microglial M1/M2 Polarisation in Rats with Spinal Cord Injury.

机构信息

The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu 730030, China.

Department of Orthopedics, Lanzhou University Second Hospital, Lanzhou, Gansu 730030, China.

出版信息

Mediators Inflamm. 2022 Aug 4;2022:2579003. doi: 10.1155/2022/2579003. eCollection 2022.

DOI:10.1155/2022/2579003
PMID:35966334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9371824/
Abstract

Spinal cord injury (SCI) is a highly disabling disorder for which few effective treatments are available. Grape seed proanthocyanidins (GSPs) are polyphenolic compounds with various biological activities. In our preliminary experiment, GSP promoted functional recovery in rats with SCI, but the mechanism remains unclear. Therefore, we explored the protective effects of GSP on SCI and its possible underlying mechanisms. We found that GSP promoted locomotor recovery, reduced neuronal apoptosis, increased neuronal preservation, and regulated microglial polarisation . We also performed studies to verify the effects of GSP on neuronal protection and microglial polarisation and their potential mechanisms. We found that GSP regulated microglial polarisation and inhibited apoptosis in PC12 cells induced by M1-BV2 cells through the Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa B (NF-B) and phosphatidylinositol 3-kinase/serine threonine kinase (PI3K/AKT) signaling pathways. This suggests that GSP regulates microglial polarisation and prevents neuronal apoptosis, possibly by the TLR4-mediated NF-B and PI3K/AKT signaling pathways.

摘要

脊髓损伤（SCI）是一种高度致残的疾病，目前几乎没有有效的治疗方法。葡萄籽原花青素（GSP）是具有多种生物学活性的多酚化合物。在我们的初步实验中，GSP 促进了 SCI 大鼠的功能恢复，但机制尚不清楚。因此，我们探讨了 GSP 对 SCI 的保护作用及其可能的机制。我们发现 GSP 促进运动功能恢复，减少神经元凋亡，增加神经元存活，并调节小胶质细胞极化。我们还进行了研究，以验证 GSP 对神经元保护和小胶质细胞极化的作用及其潜在机制。我们发现 GSP 通过 Toll 样受体 4-（TLR4-）介导的核因子 kappa B（NF-B）和磷脂酰肌醇 3-激酶/丝氨酸苏氨酸激酶（PI3K/AKT）信号通路调节 M1-BV2 细胞诱导的 PC12 细胞中的小胶质细胞极化和抑制细胞凋亡。这表明 GSP 通过 TLR4 介导的 NF-B 和 PI3K/AKT 信号通路调节小胶质细胞极化并防止神经元凋亡。

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