热应激对急性肺损伤保护作用机制研究  

Protecting mechanism of heat stress in treatment of acute lung injury

作　　者：张民[1] 熊仁平[1] 陈星云[1] 赵艳[1] 李平[1] 刘苹[1] 周元国[1] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所、创伤、烧伤与复合伤国家重点实验室分子生物学中心,重庆400042

出　　处：《中华创伤杂志》2008年第6期465-469,共5页Chinese Journal of Trauma

基　　金：高等学校全国优秀博士论文作者专项基金资助项目（200156）;国家自然科学基金资助项目（30470988） 志谢感谢第三军医大学附属大坪医院野战外科研究所病理科向德兵副主任和杜鹃技师在病理制片中的大力协助

摘　　要：目的探讨热应激预处理对急性肺损伤（acute lunginjury，ALI）保护作用的机制。方法观察热应激前后小鼠油酸ALI肺组织中糖皮质激素受体（GR）的含量、配体结合力和亲和力以及热休克蛋白（heat shock protein，Hsp）70，90的动态变化。结果热应激对小鼠肺损伤有显著的保护作用，Western blotting显示其GR水平基本维持稳定，而Hsp70、Hsp90呈进行性升高。配体结合试验显示热应激对伤后GR的Bmax和Kd的变化无明显影响。结论热应激对小鼠急性肺损伤的保护作用可能与维持GR稳定和提高Hsp70、Hsp90的水平有关。Objective To investigate the protecting mechanism of heat stress pretreatment on acute lung injury （ALI）. Methods The oleic acid ALl mouse model was built to dynamically observe the binding capacity and the binding affinity of glucocorticoid receptor （GR） , the levels of GR, heat shock protein 90 （Hsp90） and Hsp70 before and after hyperthermic stress pretreatment. Results Heat stress pretreatment had significant protective effect on ALI. Western blotting showed insignificant changes of GR levels but progressive increase of level of Hsp70 and Hsp90. Heat stress pretreatment exerted insignificant effect on Bmax and Kd of GR, shown by radio ligand binding assay after ALl. Conclusion The protective effects of heat stress pretreatment on ALl of mouse may relate to its ability of keeping stable GR level and increasing levels of Hsp70 and Hsp90.

关 键 词：糖皮质激素类 受体 细胞表面 热休克蛋白质类 热应激 

分 类 号：R563[医药卫生—呼吸系统]