地塞米松诱导胸腺细胞凋亡在神经免疫性疾病研究中的意义(英文)

Significance of dexamethasone-induced apoptosis of thymocytes in immuno neurological diseases

目的观察地塞米松诱导胸腺细胞caspase-3蛋白与p38MAPK的表达变化,探讨地塞米松诱导胸腺细胞凋亡在神经免疫性疾病研究中的意义。方法采取体外细胞培养Balb/c小鼠(体质量20g左右的Balb/c小鼠,雌雄不限)胸腺细胞的方法,制备地塞米松诱导的细胞凋亡模型,通过流式细胞仪观察凋亡细胞数量的变化情况。运用Westernblotting技术检测地塞米松处理的Balb/c小鼠胸腺细胞0,30,60,180min时相点caspase-3蛋白与p38MAPK的表达变化。结果地塞米松可以诱导Balb/c小鼠胸腺细胞发生凋亡,发生的比例是21.75%。随后的westernblot检测显示,伤后即刻p38MAPK开始表达,并在60min达到高峰,随后有所减弱。而caspase-3蛋白的表达开始较弱呈逐渐升高的趋势,一直持续至伤后180min。结论p38MAPK信号通路在地塞米松诱导的Balb/c小鼠胸腺细胞凋亡过程中起重要作用。

Aim To investigate the expression of p38MAPK and caspase 3 in dexamethasone induced apoptosis of thymocytes and explore the significance of dexamethasone induced apoptosis of thymocytes in immuno neurological diseases.Methods The mouse thymocyte model of apoptosis was induced by dexamethasone. The apoptosis ratio was observed with flow cytometry technique. The changes of caspase 3 protein and the expression of p38MAPK proteins were detected by western blotting at 0,30,60 and 180 min after dexamethasone induced thymocytes apoptosis.Results The apoptosis ratio was 21.75%.There was expression of caspase 3 at 0 min after dexamethasone inducing,then was gradually increased following time lapse,kept high till 180 min.The expression of p38MAPK was detected immediately, and reached peak at 60 min, then decreased at 180 min after dexamethasone treatment.Conclusion p38MAPK signal passage plays an important role in dexamethasone induced thymocytes apoptosis.