摘要
目的通过调节热休克蛋白70(HSP70)的表达,观察HSP70在三氧化二砷(ATO)诱导胶质瘤细胞U251MG死亡中的作用。方法台盼蓝染色用来评价细胞的活性,免疫印迹分析HSP70和Caspase-3表达情况,进一步使用热休克蛋白抑制剂KNK437和热激的方法调节HSP70的水平,观察ATO在不同HSP70水平对U251MG死亡的影响。结果 ATO诱导U251MG细胞的死亡,伴有HSP70的表达;应用KNK437明显增加ATO诱导U251MG细胞的死亡和凋亡蛋白Caspase-3表达;热激明显抑制ATO诱导U251MG细胞的死亡。结论 HSP70在ATO诱导胶质瘤细胞U251MG死亡中起保护作用,KNK437可能在ATO治疗胶质瘤中起协同作用。
Objective To investigate the role of heat shock protein70（HSP70） in U251MG glioma cells death induced by arsenic trioxide（ATO） by regulating the expression of HSP70.Methods Trypan blue exclusion assay was used to evaluate the cell viability.Western blot was employed to detect the expression of HSP70 and Caspase 3 induced by ATO.And then heat pre-treatment and HSPs inhibitor,KNK437,were used to regulate the expression of HSP70 to observe the effect of ATO on U251MG glioma cells death at different expression levels of HSP70.ResultsATO induced U251MG glioma cell death with the expression of HSP70.It was shown that KNK437 could significantly enhance the cell death and Caspase-3 cleavage induced by ATO,while heat pre-treatment inhibited the effect of ATO.Conclusion HSP70 plays a protective role in ATO-induced cell death in glioma.KNK437 may have a synergistic effect with ATO on glioma treatment.
出处
《中华神经外科疾病研究杂志》
CAS
2012年第5期423-426,共4页
Chinese Journal of Neurosurgical Disease Research
基金
哈尔滨医科大学科第一附属医院科研基金资助项目(2009Y11)
