二甲双胍减轻氧糖剥夺/复糖复氧所诱导的小胶质细胞炎性反应

Metformin reduces the oxygen-glucose deprivation and reoxygenation-induced microglial inflammation

目的 :研究二甲双胍在氧糖剥夺/复糖复氧所致小胶质细胞炎性反应中的作用。方法 :建立氧糖剥夺/复糖复氧模型诱导小胶质细胞(BV-2细胞株)的活化,给予不同浓度(0.02、0.20、2.00 mmol/L)的二甲双胍预处理BV-2细胞,通过MTT活性和乳酸脱氢酶活性检测确定二甲双胍的有效浓度;通过酶联免疫吸附试验测定细胞上清炎性因子白介素(IL)-1β的含量,免疫荧光检测细胞表面分子CD11b的表达及蛋白免疫印迹法分析胞核蛋白κB的表达。结果:二甲双胍(2.00 mmol/L)能够减少氧糖剥夺/复糖复氧模型诱导的BV-2细胞乳酸脱氢酶的释放并增加MTT的活性,降低细胞表面分子CD11b的表达,抑制胞核蛋白κB的核转位,减少IL-1β的生成与释放。结论:二甲双胍能够减轻氧糖剥夺/复糖复氧所致小胶质细胞的炎性反应。

Objective：To study the effects of metformin on oxygen glucose deprivation and reoxygenation（OGD / R）-induced microglial inflammatory reaction. Methods： To establish the OGD / R model of microglia（BV-2 cells）, BV-2 cells were pretreated with different concentrations（0.02, 0.20 and 2.00 mmol / L） of metformin, the effective concentration of metformin was determined by MTT and lactate dehydrogenase（LDH） assays. The supernatant of IL-1β was determined by enzyme-linked immunosorbent assay,expressions of nuclear factor kappa B and CD11 b were analyzed by Western blot and immunofluorescence,respectively. Results：Metformin（2.00 mmol / L） decreased the release of OGD / R-induced LDH from BV-2 cells and increased MTT activity, reduced the expression of cell surface molecule CD11 b, inhibited nuclear translocation of NF-kappa B, and decreased production and release of IL-1β. Conclusion： Pretreatment with metformin could reduce OGD / R-induced microglia inflammatory response.