摘要
目的:探讨热休克蛋白在Act-D诱导肺癌GLC-82细胞凋亡中的作用,为进一步探讨HSP抗凋亡机制及肺癌生物治疗提供实验依据。方法:体外培养的肺癌GLC-82细胞于RPMI1640、10%胎牛血清、5%CO2孵育,取指数生长期细胞1×105/ml接种反应板24h,分为非热休克组(NHS)和热休克组(HS),两组分别由不同浓度(0,5,10,20μg/m1)放线菌素D(Act-D)诱导,作用4 h。采用脱氧核苷酸末端转移酶介导的dUTP缺口末端标记法(TUNEL)和3H-胸腺嘧啶脱氧核苷(3H-TdR)掺入试验检测肿瘤细胞凋亡指数(AI)及DNA合成情况。结果:HS组比NHS组凋亡指数明显下降(P<0.01);cpm值明显升高(P<0.01),呈现剂量依赖效应。结论:热休克反应对肺癌GLC-82细胞经Act-D诱导凋亡具有抑制作用,此作用与Act-D呈剂量依赖效应。
Objective:To investigate the effect on HSP on lung cancer cells GLC-82 apoptosis induced by Actinomycin-D.Methods:Lung cancer cells which were cultured in vitro were divided into NHS and HS groups before treated by Act-D.TUNEL was used to exam apoptosis index and 3H-TdR test is used to examing DNA synthsis.Results:The apoptosis index of HS group significantly decreased than that in NHS group(P0.01).And the cpm of HS group significant increase than that in NHS group(P0.01),which were depended on the dosage of Act-D.Conclusion:This paper results indicate that HSP has significant inhibition of apoptosis induced by Act-D in lung cancer cells in vitro.
出处
《陕西医学杂志》
CAS
2011年第5期544-546,共3页
Shaanxi Medical Journal