HSR对TNF-α诱导的肺癌细胞凋亡的拮抗作用

Heat Shock Response Influence on Pulmonary Carcinoma Cells in Apoptosis by TNF-α

目的 研究热休克反应（HSR）在肺癌细胞GLC-82增殖及凋亡过程中的作用，为肺癌的临床治疗提供实验参考。方法 用体外培养的肺癌细胞GLC-82细胞分为热休克（HS）组和非热休克（NHS）组，每组分为对照组和TNF-α组，TNF-α的浓度分别为25μg／L、50μg／L和100μg／L（T1～T3），采用脱氧核苷酸末端转移酶介导的dUTP缺口末端标记法（TUNEL）检测肿瘤细胞凋亡指数（AI）；噻唑蓝比色法（MTT、）检测肿瘤细胞的细胞增殖情况；以3H-TdR掺入试验检测肿瘤细胞的DNA合成情况。结果 HS组细胞凋亡百分率明显减少；MTT显示HSR可以使细胞GLC-82抵抗TNF-α的细胞毒作用明显增强，促进细胞增殖；DNA合成明显增加；且与TNF-α呈剂量依赖效应。结论 HSR在肺癌细胞GLC-82生长增殖过程中起促进作用，而对细胞凋亡起拮抗作用。

Objective To explore the effect of Heat shock response （HSR） on cells proliferation and apoptosis of pulmonary carcinoma, and provide laboratory reference in clinical therapy of pulmonary carcinoma. Methods Pulmonary carcinoma cells treated with TNF-α are divided two groups, heat shock treated and heat shock untreated. MTT and 3^H - TdR are used for examined cell growth inhibition and DNA synthesis cell , apoptosis was evaluated by TUNEL. Results The effect of cells proliferation of HS group is more significantly enhanced than NHS one, which is depended on the dose of TNF-α. On the other hand, the AI of apoptosis in HS group are more decreased than the NHS one. Conclusions The results indicated that HSR has significant inhibition of apoptosis by TNF-α in pulmonary carcinoma cells.