摘要
目的观察体外诱导热应激反应对IL 6所致中性粒细胞凋亡障碍的影响。方法将 14例健康人的中性粒细胞分成 6份 ,其中 1份作为对照组 ,其余 5份应用热休克或氯化镉诱导热应激反应后与培养液或IL 6共同孵育 ,分为热休克组、氯化镉组、IL 6组、IL 6 +热休克组及IL 6 +氯化镉组。各组于热应激反应诱导后 3、2 0h分别测定中性粒细胞热休克蛋白 (HSP70 )的表达及凋亡率。结果热休克与氯化镉均可诱导热应激反应 ,细胞内HSP70表达增加 ;热应激反应促进凋亡 ,IL 6导致中性粒细胞凋亡抑制 ,IL 6不影响热应激反应对中性粒细胞的促凋亡作用。结论热应激反应促进凋亡并可逆转IL 6对其凋亡的抑制作用 。
Objective To study the effect of heat stress response on interleukin-6(IL-6) induced inhibition of neutrophil apoptosis. Methods Neutrophils from each of 14 healthy volunteers were divided into 6 parts, one part was served as control group, and the other parts were induced by heat shock or cadmium for heat stress response. Finally, the 5 parts were incubated with IL-6 or culture medium and named as heat shock group, cadmium group, IL-6 group, IL-6+ heat shock group, IL-6+ cadmium group respectively. After 3 h of heat stress induction and 20 h of incubation, the heat shock protein (HSP70) expression and the rate of apoptosis were detected in the PMNs respectively. Results Heat stress response was successfully induced in the groups exposed to heat shock or cadmium; IL-6 inhibited neutrophil apoptosis, but heat stress response accelerated neutrophil apoptosis and the effect was not interfered with IL-6. Conclusion Heat stress response can promote apoptosis and reverse IL-6 induced inhibition of apoptosis in PMNs, indicating that heat stress response may be one of anti-inflammatory roles.
出处
《上海第二医科大学学报》
CSCD
2004年第11期891-893,912,共4页
Acta Universitatis Medicinalis Secondae Shanghai
基金
上海市卫生局基金 (0 340 50 )资助项目
