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【目的】研究特异性p38分裂原激活的蛋白激酶 (MAPK)抑制剂SB2 0 35 80对低钾诱导的小脑颗粒神经元凋亡的作用。【方法】把体外培养的小脑颗粒神经元从含去极化浓度钾离子 (KCl 2 5mmol·L-1)的培养基中转移至低钾培养基 (KCl5mmol·L-1)中诱导神经元凋亡。凝胶电泳分析DNA片段 ,SAPK/JNK分析盒测定c JunN 末端蛋白激酶 (JNK)活性。【结果】低钾诱导小脑颗粒神经元的具有典型形态学和生化特征的凋亡。特异性的p38MAPK抑制剂SB2 0 35 80通过抑制细胞凋亡 ,促进低钾环境中培养的小脑颗粒神经元存活。这种保护作用具有浓度依赖性。培养于低钾环境中的颗粒神经元 ,c Jun表达和磷酸化水平升高了 ,且激活了JNK活性。当小脑颗粒神经元生长在含SB2 0 35 80 2 5 μmol·L-1的低钾培养基中 ,c Jun表达、磷酸化水平和JNK活性都明显降低。【结论】SB2 0 35 80抑制JNK活性 ,降低c Jun的磷酸化而对低钾培养的小脑颗粒神经元具有保护作用
【Aim】 To investigate the effect of SB203580, a specific inhibitor of p38 mitogen-activated protein kinase (MAPK), on apoptosis of cerebellar granule neurons induced by hypokalemia. 【Methods】 Cerebellar granule neurons cultured in vitro were transferred into KCl5mmol·L-1 medium containing KCl 2 5mmol·L-1 to induce neuronal apoptosis Death. DNA fragments were analyzed by gel electrophoresis and cNNK activity was measured using a SAPK / JNK assay cassette. [Results] Hypokalemia induced apoptosis of cerebellar granule neurons with typical morphological and biochemical characteristics. The specific p38 MAPK inhibitor SB2 0 35 80 promotes the survival of cerebellar granule neurons cultured in hypokalemia by inhibiting apoptosis. This protective effect is concentration-dependent. Granulocyte neurons cultured in a hypoxic environment have elevated c Jun expression and phosphorylation, and have activated JNK activity. When cerebellar granule neurons grew in low potassium medium containing SB20358025μmol·L-1, c Jun expression, phosphorylation and JNK activity were significantly decreased. 【Conclusion】 SB2 0 35 80 inhibits the activity of JNK, decreases the phosphorylation of c Jun, and protects cerebellar granule neurons cultured in hypokalemia