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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。
Objective To investigate the expression of caspase-3 protein and p38MAPK in dexamethasone-induced thymus cells and to explore the significance of dexamethasone-induced thymocyte apoptosis in the study of neuroimmune diseases. Methods Apoptosis model induced by dexamethasone was prepared by culturing Balb / c mice (Balb / c mice weighing about 20g, male or female) thymocytes in vitro. The apoptosis was observed by flow cytometry Changes in the number of cells. Western blotting was used to detect the expression of caspase-3 protein and p38MAPK in dexamethasone-treated Balb / c mouse thymocytes at 0, 30, 60 and 180 min. Results Dexamethasone induced apoptosis in the thymocytes of Balb / c mice at a rate of 21.75%. Subsequent western blot showed that p38MAPK started to express immediately after injury and peaked at 60 min, then weakened. However, the expression of caspase-3 protein began to weaken and gradually increased until 180min after injury. Conclusion p38 MAPK signaling pathway plays an important role in dexamethasone-induced apoptosis in Balb / c mouse thymocytes.