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目的观察14,15-环氧化二十碳三烯酸(14,15-EET)对糖氧剥夺/复氧(OGD/R)诱导的BV2小鼠小胶质细胞炎症反应的影响。方法将BV2细胞随机分为空白对照组、溶剂对照组及14,15-EET干预组。在14,15-EET的干预作用下,利用酶联免疫吸附测定(ELISA)法测定BV2细胞OGD1h后复糖复氧0,3,6,12,24 h时细胞培养液中肿瘤坏死因子-α(TNF-α)的浓度;并用噻唑蓝(MTT)实验检测其各时间点细胞活性的改变。同样条件下,Transwell细胞迁移实验用来观察BV2细胞的迁移能力变化。结果与溶剂对照组比较,14,15-EET干预组BV2细胞培养液中分泌的炎症因子浓度显著减少;细胞活性明显降低;迁移能力显著减弱。以上结果均以OGD1h/R12h最具统计学意义。结论 14,15-EET对BV2细胞OGD再灌注损伤后的炎症反应具有一定的抑制作用。
Objective To observe the effect of 14,15-epoxidation of eicosatetraenoic acid (14,15-EET) on microglia inflammatory response induced by OGD / R in BV2 mice. Methods BV2 cells were randomly divided into blank control group, solvent control group and 14,15-EET intervention group. The effects of 14,15-EET on the expression of tumor necrosis factor-α (TNF-α) in BV2 cells were detected by enzyme linked immunosorbent assay (ELISA) at 0,3,6,12,24 h after OGD1h (TNF-α). The cell viability was measured by MTT assay at each time point. Under the same conditions, Transwell cell migration assay was used to observe the change of BV2 cell migration ability. Results Compared with the solvent control group, the concentrations of inflammatory cytokines secreted by BV2 cells in 14,15-EET intervention group were significantly decreased; the cell viability was significantly decreased; and the migration ability was significantly weakened. The above results were OGD1h / R12h the most statistically significant. Conclusion 14,15-EET can inhibit the inflammatory response of BV2 cells after OGD reperfusion injury.