甲酰肽受体-2促进LPS诱导的BV-2细胞炎症反应

Formyl peptide receptor-2 enhances inflammatory response induced by lipopolysaccharide in BV-2 cells

目的考察脂多糖(lipopolysaccharide,LPS)激活的BV-2细胞中甲酰肽受体-2(formyl peptide receptor-2,FPR2)的表达及其对细胞炎症反应的作用。方法 1 mg·L^(-1)的LPS刺激BV-2细胞12 h,建立体外小胶质细胞炎症模型。Western blot法检测FPR2的表达;分别用FPR2特异性激动剂MMK^(-1)和拮抗剂Boc-2孵育LPS-BV-2细胞后,ELISA法检测肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白介素1β(interleukin^(-1)β,IL^(-1)β)的分泌情况;Western blot法检测下游信号分子NF-κB的磷酸化;Transwell小室法考察LPS-BV-2细胞的迁移情况。结果 LPS可使BV-2细胞上的FPR2表达上调,并激活NF-κB。与LPS组比较,激动剂MMK^(-1)可促进LPS-BV-2细胞的TNF-α、IL^(-1)β的分泌和趋化,拮抗剂Boc-2可抑制这些反应。结论 LPS可诱导BV-2细胞膜表面FPR2表达上调,FPR2可使LPS诱发的炎症反应增强。

Aim To investigate the expression of formyl peptide receptor-2( FPR2) in lipopolysaccharide ( LPS)-induced-BV-2 cells, and detect FPR2's influence on inflammatory response induced by LPS.Methods After 1 mg·L^(-1) LPS acting on BV-2 cells at 12 h,the extrinsic inflammatory model was established. We used the Western blot assay to test the levels of FPR2 protein. And the expressions of phosphorylated NF-κB,TNF-α and IL^(-1)β were investigated when the LPS-induced-BV-2 was incubated with FPR2's agonist MMK^(-1) and antagonist Boc-2. Transwell assay was also used to detect the LPS-inducedBV-2 migration induced by MMK^(-1) and Boc-2. Results LPS up-regulated the expression of FPR2,and when its agonist was acted on LPS-induced-BV-2,the levels of phosphorylated NF-κB, TNF-α and IL^(-1)βwere significantly higher than those of LPS group. In addition,the chemotaxis of LPS-induced-BV-2 also increased by MMK^(-1). These effects were abolished by Boc-2. Conclusions LPS can increase the expression of FPR2 on BV-2 cells,and FPR2 enhances the inflammatory response induced by LPS.