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Bcl-2 对脂多糖诱导的皮质神经干细胞神经炎症的神经保护作用。

Neuroprotective Effect of Bcl-2 on Lipopolysaccharide-Induced Neuroinflammation in Cortical Neural Stem Cells.

机构信息

Biomedical Research Institute and Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul 04763, Korea.

出版信息

Int J Mol Sci. 2022 Jun 7;23(12):6399. doi: 10.3390/ijms23126399.

DOI:10.3390/ijms23126399
PMID:35742844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9223771/
Abstract

Neuroinflammation is involved in the pathogenesis of neurodegenerative diseases due to increased levels of pro-inflammatory cytokines in the central nervous system (CNS). Chronic neuroinflammation induced by neurotoxic molecules accelerates neuronal damage. B-cell lymphoma 2 (Bcl-2) is generally accepted to be an important anti-apoptotic factor. However, the role of Bcl-2 in neuroprotection against neuroinflammation remains to be determined. The purpose of this study was to investigate the neuroprotective effect of Bcl-2 on lipopolysaccharide (LPS)-induced neuroinflammation in cortical neural stem cells (NSCs). LPS decreased mRNA and protein levels of Tuj-1, a neuron marker, and also suppressed neurite outgrowth, indicating that LPS results in inhibition of neuronal differentiation of NSCs. Furthermore, LPS treatment inhibited Bcl-2 expression during neuronal differentiation; inhibition of neuronal differentiation by LPS was rescued by Bcl-2 overexpression. LPS-induced pro-inflammatory cytokines, including interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α), were decreased by Bcl-2 overexpression. Conversely, Bcl-2 siRNA increased the LPS-induced levels of IL-6 and TNF-α, and decreased neuronal differentiation of NSCs, raising the possibility that Bcl-2 mediates neuronal differentiation by inhibiting the LPS-induced inflammatory response in NSC. These results suggest that Bcl-2 has a neuroprotective effect by inhibiting the LPS-induced inflammatory response in NSCs.

摘要

神经炎症参与神经退行性疾病的发病机制，是由于中枢神经系统（CNS）中促炎细胞因子水平升高所致。神经毒性分子引起的慢性神经炎症加速神经元损伤。B 细胞淋巴瘤 2（Bcl-2）通常被认为是一种重要的抗细胞凋亡因子。然而，Bcl-2 在神经炎症保护中的作用仍有待确定。本研究旨在探讨 Bcl-2 对脂多糖（LPS）诱导的皮质神经干细胞（NSCs）神经炎症的神经保护作用。LPS 降低了神经元标志物 Tuj-1 的 mRNA 和蛋白水平，并抑制了突起生长，表明 LPS 导致 NSCs 的神经元分化受到抑制。此外，LPS 处理抑制了神经元分化过程中的 Bcl-2 表达；Bcl-2 的过表达挽救了 LPS 诱导的神经元分化抑制。Bcl-2 过表达降低了 LPS 诱导的促炎细胞因子，包括白细胞介素（IL）-6 和肿瘤坏死因子-α（TNF-α）。相反，Bcl-2 siRNA 增加了 LPS 诱导的 IL-6 和 TNF-α水平，并减少了 NSCs 的神经元分化，这表明 Bcl-2 通过抑制 NSCs 中 LPS 诱导的炎症反应来介导神经元分化。这些结果表明，Bcl-2 通过抑制 NSCs 中 LPS 诱导的炎症反应发挥神经保护作用。

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