左旋丁基苯酞抑制氧糖剥夺/复氧所致原代培养小鼠脑胶质细胞内NF-κB和IκB-α蛋白表达

L-3-n-butylphthalide inhibits expression of nuclear factor-κB and IκB-α in primary cultured murine brain glial cells following oxygen-glucose deprivation/reoxygenation

目的观察左旋丁基苯酞(l-NBP)对原代培养小鼠脑胶质细胞氧糖剥夺/复氧(OGD/R)后NF-κB、IκB-α蛋白表达的影响。方法体外培养小鼠脑胶质细胞,建立细胞OGD/R损伤模型。将胶质细胞分为5组:正常对照(NC)组、OGD 24h/R 24h组、l-NBP 20、100及500μmol/L组。Western-blot检测各组细胞核蛋白中NF-κB蛋白表达和胞质蛋白中IκB-α蛋白降解情况。结果OGD 24h/R 24h组NF-κB蛋白表达较NC组明显增加(P<0.01);l-NBP 100和500μmol/L组NF-κB蛋白表达较OGD 24h/R 24h组明显下降(P<0.01)。OGD 24h/R 24h组IκB-α蛋白降解比NC组增多(P<0.01);l-NBP 500μmol/L组IκB-α蛋白降解较OGD 24h/R 24h组明显减少(P<0.05)。结论l-NBP能抑制脑胶质细胞OGD/R后炎症反应,表现为减少IκB-α蛋白降解,抑制NF-κB活化。

Objective To observe the effect of 1-3-n-butylphthalide（1-NBP）on the of nuclear factor-KB and IKB-α in primary cultured murine brain glial cells following oxygen-glucose deprivation/reoxygenation （OGD/R）. Methods Cultured mouse brain glial ceils in vitro and established OGD/R model. Glial ceils were divided into five groups ： normal control（ NC ） group, OGD 24 h/R 24 h group, 1-NBP 20 μmoL/L group, 1-NBP 100 μmoL/L group, 1-NBP 500 μmol/L group. The protein expression of NF-KB in nuclear and IKB-α in endochylema were analyzed by Western blot. Results Comparing with NC group, OGD 24 h/R 24 h group showed a significantly higher expression of NF-KB （P 〈0. 01 ）. The expression of NF-KB in 1-NBP 100μmoL/L group and 1-NBP 500 μmoL/L group were evidently lower than that in OGD 24 h/R 24 h group（P 〈0. 01 ）. The degradation of IKB-α in OGD 24 h/R 24 h group was significantly higher than that in NC group（P 〈0. 01 ）. It was evident that the degradation of IKB-α in 1-NBP 500 Ixmol/L group was lower than that in OGD 24 h/R 24 h group（P 〈 0. 05 ）. Conclusion 1-NBP can inhibit seeondary inflammation of glial cells following OGD/R by decreasing the degradation of IKB-α and inhibit- ting activation of NF-KB.