热应激反应对中性粒细胞凋亡及呼吸爆发功能的影响

Effects of heat stress response on neutrophil apoptosis and respiratory burst function

目的观察体外诱导热应激反应对中性粒细胞凋亡及呼吸爆发功能的影响。方法18例健康者中性粒细胞每例随机分为三份。其中1份作为对照组,其余2份分别应用热休克或氯化镉诱导热应激反应后与培养液共同孵育,并分别作为热休克组和氯化镉组。于热应激反应诱导后0、2、3、4、6 h,运用PCR技术和流式细胞仪分别测定各组中性粒细胞热休克蛋白(HSP70)的表达及呼吸爆发功能;于热应激反应后24 h,应用荧光染色法和流式细胞仪DNA倍体分析法观察、检测细胞凋亡情况。结果热休克组和氯化镉组热应激诱导后各时段中性粒细胞HSP70表达及24 h的细胞凋亡率均明显高于对照组(P<0.01);热休克组和氯化镉组热应激诱导后4 h和6 h时,中性粒细胞活性氧生成明显低于对照组(P<0.01)。结论热应激反应促进中性粒细胞凋亡并减少活性氧释放。提示热应激反应可能参与机体的抗炎作用机制。

To explore effects of heat stress response on neutrophil apoptosis and respiratory burst function. Methods Neutrophils from each of 18 healthy volunteers were divided into 3 parts, and one part was served as control group, and the other two parts were induced by heat shock or cadmium chloride for heat stress response and named as heat shock group and cadmium chloride group. The neutrophils were incubated in culture medium. At 0, 2, 3, 4, and 6 h following heat stress induction, the heat shock protein （HSPT0） expression and the respiratory burst were detected in the neutrophils respectively by using PCR technique and flow cytometer. Level of apoptosis was observed by immuno-fluorescence and flow cytometer DNA ploid at 24 h after heat stress induction. Results In the heat shock and cadmium chloride groups, HSP70 expression at each time point and cell apoptosis at 24 h were significantly higher than those of control group （P 〈 0.01）. At 4 and 6 h, reactive oxgen speices produced significantly less in two experimental groups than in control group （P 〈 0.01）. Conclusion Heat stress response can promote apoptosis and decrease respiratory burst activity in neutrophils, indicating that heat stress response may be one of anti-inflammatory roles.