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瑞芬太尼抑制 BV2 小胶质细胞的炎症反应,并保护 PC12 细胞免受小胶质细胞激活引起的损伤。

Remifentanil inhibits the inflammatory response of BV2 microglia and protects PC12 cells from damage caused by microglia activation.

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.

出版信息

Bioengineered. 2022 May;13(5):13944-13955. doi: 10.1080/21655979.2022.2080421.

DOI:10.1080/21655979.2022.2080421
PMID:35726401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275917/
Abstract

Microglia acts as a critical player in neuroinflammation and neuronal injury. Remifentanil (Rem) has been reported to exert anti-inflammatory activity in several types of diseases. However, the role of Rem in microglia-mediated neuroinflammation is unclear. The present study was designed to investigate the effects of Rem against lipopolysaccharide (LPS)-activated BV2 microglial and PC12 cell induced by activated BV2 microglia. Cell proliferative ability was assessed with cell counting kit-8 assay and cellular morphology was observed. ELISA assay was used to measure the expressions of PGE2 and inflammatory factors. The contents of p-NF-KB p65, p-IKKα/β, and COX2 were evaluated with the aid of western blot. The levels of NO and iNOS were assessed with Griess assay, qRT-PCR, and western blot. In addition, Tunel assay and western blot were performed to assess cell apoptosis. The data revealed that Rem alleviated BV2 microglial morphological injury induced by LPS. Furthermore, Rem suppressed inflammatory releases, iNOS, NO and PGE2 stimulated by LPS in activated BV2 cells. Moreover, Rem suppressed PC12 cell injury, the generations of inflammatory factors and cell apoptosis triggered by inflammatory mediators secreted from activated BV2 cells. These results suggest that Rem exhibited anti-neuroinflammatory activity in protecting PC12 cells against injury derived from LPS-stimulated BV2 microglia.

摘要

小胶质细胞在神经炎症和神经元损伤中起着关键作用。瑞芬太尼(Rem)已被报道在几种疾病中具有抗炎活性。然而,Rem 在小胶质细胞介导的神经炎症中的作用尚不清楚。本研究旨在探讨 Rem 对脂多糖(LPS)激活的 BV2 小胶质细胞和由激活的 BV2 小胶质细胞诱导的 PC12 细胞的影响。用细胞计数试剂盒-8 法评估细胞增殖能力,观察细胞形态。采用 ELISA 法测定 PGE2 和炎症因子的表达。用 Western blot 法评价 p-NF-KB p65、p-IKKα/β 和 COX2 的含量。用 Griess 法、qRT-PCR 和 Western blot 法测定 NO 和 iNOS 的水平。此外,采用 Tunel assay 和 Western blot 法评估细胞凋亡。结果表明,Rem 减轻了 LPS 诱导的 BV2 小胶质细胞形态损伤。此外,Rem 抑制了 LPS 激活的 BV2 细胞中炎症因子 iNOS、NO 和 PGE2 的释放。此外,Rem 抑制了由激活的 BV2 细胞分泌的炎症介质触发的 PC12 细胞损伤、炎症因子的产生和细胞凋亡。这些结果表明,Rem 在保护 PC12 细胞免受 LPS 刺激的 BV2 小胶质细胞损伤方面表现出抗炎活性。

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