半胱氨酸蛋白酶3和白细胞介素8在高氧暴露下早产大鼠肺组织中的动态表达及其意义  

Temporal expression and significance of caspase-3 and interlenkin-8 in the lungs of preterm rats exposed to hyperoxia

作　　者：刘伟[1] 常立文[1] 李文斌[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院儿科,武汉430030

出　　处：《中华儿科杂志》2008年第3期229-233,共5页Chinese Journal of Pediatrics

基　　金：国家自然科学基金资助项目（30471824）;国家“十五”科技攻关项目（2004BA720A11）

摘　　要：目的 探讨半胱氨酸蛋白酶-3（Caspase-3）及白细胞介素-8（IL-8）在早产大鼠高氧肺损伤中的动态表达及其意义。方法孕21d的SD早产大鼠生后第2天，随机分为空气组和高氧组（均n=40）。高氧组大鼠予以85％高氧持续暴露，空气组大鼠置于空气中。于暴露1、4、7、14和21d每组各处死8只大鼠，收集肺组织标本，苏木精咿红染色观察肺组织病理形态学变化，双抗夹心ELISA法检测IL-8含量，免疫组化和Western blot检测Caspase-3表达。结果高氧暴露后肺泡腔内可见有坏死脱落细胞、炎症细胞渗出增多、间质水肿，肺组织结构紊乱，肺泡形成明显滞后，肺泡结构简单化和囊泡化；与空气对照组比较，高氧暴露4、7和14d肺组织Caspase-3和IL-8含量均明显增高（P〈0．01）。结论在高氧所致早产大鼠肺损伤中细胞凋亡和坏死共存，两者共同参与了早产大鼠高氧肺损伤的病理过程。Objective To explore the temporal expression and significance of Caspase-3 and interleukin-8（ IL-8 ）in hyperoxia-indueed lung injury in preterm rats. Methods Two-day-old Sprague-Dawley preterm rats were randomly divided into Air group and Hyperoxia group （each rats in each group）. Rats in the Hyperoxia group were exposed to 85% O2 , while rats in the Air group were exposed to air. The rats in each group were sacrificed at 1,4, 7, 14 and 21 days after exposure （ 8 rats at each time point）, and lung tissues were collected. Pathomorphology of lungs was observed by hematoxylin-eosine staining. The contents of IL-8 in the homogenate of lungs were detected using ELISA. The expression of Caspase-3 was detected by immunohistochemistry and Western blot. Results （ 1 ） Lung histopathology： after hyperoxia exposure 1 day, no significant effects on alveoli were found; but on days 4 and 7, alveolitis appeared： there were nacrotie abacission cells in alveolar space, increased inflammatory cells infiltration, lung interstitial edema; on days 14 and 21, lung structure derangement, decreased number of alveoli, simplified and vesicular lung structure, all of which showed the retardation of alveolar formation. （2） the contents of IL-8 in the homogenate of lungs had no significant change on day 1 but increased significantly on days 4, 7 and 14 compared with air control group （P 〈 0. 01 for all）. （3） Immunohistochemistry detected the expression of Caspase-3 in the lung： the intensity of Caspase-3 expression increased significantly on days 4, 7 and 14 compared with air control group （ P 〈 0. 01 ）. （4） Western blotting detected the expression of easpase-3 in the lung： the pattern of dynamic expression of Caspase-3 was similar to the restdts of immunohistochemistry. Conclusions Both apoptesis and necrosis contribute to ceil death during hyperoxia. Apoptesis and necrosis may both play an important role in hyperoxia-indueed lung injury in preterm rats.

关 键 词：半胱氨酸天冬氨酸蛋白酶 白细胞介素8 高氧症 肺疾病 婴儿 早产 

分 类 号：R686[医药卫生—骨科学]