首页> 外文期刊>Bosnian Journal of Basic Medical Sciences >Possible involvement of calcium channels and plasma membrane receptors on Staurosporine-induced neurite outgrowth
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Possible involvement of calcium channels and plasma membrane receptors on Staurosporine-induced neurite outgrowth

机译:钙通道和质膜受体可能参与星形孢菌素诱导的神经突增生

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Staurosporine as a protein kinases inhibitor induced cell death or neurite outgrowth in PC12 cells. We investigated the involvement of calcium channel and plasma membrane receptors on staurosporine inducing neurite outgrowth in PC12 cells. PC12 cells were preincubated with NMDA receptor inhibitors (1.8 mM ketamine and 1μM MK801, treatment 1) or L-Type Calcium channels (100 μM nifedipine and 100 μM flavoxate hydrochloride, treatment 2) or calcium-calmoduline kinasses (10 μM trifluoprazine, treatment 3) and nifedipine, MK801, flavoxate hydrochloride and ketamine (treatment4) or without pretreatments (control). Then, the cells were cultured in RPMI culture medium containing 214nM staurosporine for induction of neurite outgrowth. The percentage of Cell cytotoxicity and apoptotic index was assessed. Total neurite length (TNL) and fraction of cell differentiation were assessed. After 24h, the percentage of cell cytotoxicity were increased in treatments 1, 2 and 4 compared with control (p
机译:星形孢菌素作为一种蛋白激酶抑制剂可诱导PC12细胞死亡或神经突生长。我们调查了钙通道和质膜受体在星形孢菌素诱导PC12细胞中神经突增生中的参与。将PC12细胞与NMDA受体抑制剂(1.8 mM氯胺酮和1μMMK801,处理1)或L型钙通道(100μM硝苯地平和100μM盐酸黄酮酸盐,处理2)或钙钙调蛋白激酶(10μM三氟哌嗪,处理3)预孵育),硝苯地平,MK801,盐酸黄酮酸和氯胺酮(治疗4)或不进行预处理(对照)。然后,将细胞在含有214nM星形孢菌素的RPMI培养基中培养以诱导神经突生长。评估细胞毒性百分比和细胞凋亡指数。评估总神经突长度(TNL)和细胞分化分数。 24小时后,与对照组相比,治疗1、2和4的细胞毒性百分比增加(p

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