中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2009年
4期
362-364
,共3页
黄宇戈%余彦亮%肖芳芳%黄秀兰%矫青
黃宇戈%餘彥亮%肖芳芳%黃秀蘭%矯青
황우과%여언량%초방방%황수란%교청
泛素蛋白酶体抑制剂%MG-132%高氧%凋亡%Bax%Bcl-2
汎素蛋白酶體抑製劑%MG-132%高氧%凋亡%Bax%Bcl-2
범소단백매체억제제%MG-132%고양%조망%Bax%Bcl-2
Proteasome inhibitor%MG-132%Hyperoxia%Apoptosis%Bax%Bcl-2
目的 观察泛素蛋白酶体抑制剂MG-132对高氧肺损伤大鼠肺上皮细胞凋亡的影响并初步探讨相关机制.方法 实验采用完全随机设计.将26只SD大鼠分为4组:高氧组(n=8)、高氧+MG-132组(n=8)、空气对照组(n=5)、MG-132对照组(n=5).成功制备高氧肺损伤大鼠模型后,观察肺组织病理学改变,TUNEL法检测细胞凋亡,免疫组化法检测Bax、Bcl-2蛋白的表达并计算Bcl.2/Bax值.结果 高氧组SD大鼠肺组织可见明显急性炎症反应.高氧组、高氧+MG-132组的凋亡指数分别为66.76±7.64、34.78±4.40,明显高于空气组与MG-132对照组(14.48±1.75、12.88±1.95),但高氧+MG-132组的凋亡指数要低于高氧组,差异有显著性(P<0.05).高氧+MG-132组Bcl-2/Bax值(1.22±0.15)高于高氧组(0.87±0.11),差异有显著性(P<0.05).结论 高氧诱发肺组织细胞发生凋亡,蛋白酶体抑制剂MG-132可以通过调节Bcl-2与Bax的表达减轻高氧引起的细胞凋亡.
目的 觀察汎素蛋白酶體抑製劑MG-132對高氧肺損傷大鼠肺上皮細胞凋亡的影響併初步探討相關機製.方法 實驗採用完全隨機設計.將26隻SD大鼠分為4組:高氧組(n=8)、高氧+MG-132組(n=8)、空氣對照組(n=5)、MG-132對照組(n=5).成功製備高氧肺損傷大鼠模型後,觀察肺組織病理學改變,TUNEL法檢測細胞凋亡,免疫組化法檢測Bax、Bcl-2蛋白的錶達併計算Bcl.2/Bax值.結果 高氧組SD大鼠肺組織可見明顯急性炎癥反應.高氧組、高氧+MG-132組的凋亡指數分彆為66.76±7.64、34.78±4.40,明顯高于空氣組與MG-132對照組(14.48±1.75、12.88±1.95),但高氧+MG-132組的凋亡指數要低于高氧組,差異有顯著性(P<0.05).高氧+MG-132組Bcl-2/Bax值(1.22±0.15)高于高氧組(0.87±0.11),差異有顯著性(P<0.05).結論 高氧誘髮肺組織細胞髮生凋亡,蛋白酶體抑製劑MG-132可以通過調節Bcl-2與Bax的錶達減輕高氧引起的細胞凋亡.
목적 관찰범소단백매체억제제MG-132대고양폐손상대서폐상피세포조망적영향병초보탐토상관궤제.방법 실험채용완전수궤설계.장26지SD대서분위4조:고양조(n=8)、고양+MG-132조(n=8)、공기대조조(n=5)、MG-132대조조(n=5).성공제비고양폐손상대서모형후,관찰폐조직병이학개변,TUNEL법검측세포조망,면역조화법검측Bax、Bcl-2단백적표체병계산Bcl.2/Bax치.결과 고양조SD대서폐조직가견명현급성염증반응.고양조、고양+MG-132조적조망지수분별위66.76±7.64、34.78±4.40,명현고우공기조여MG-132대조조(14.48±1.75、12.88±1.95),단고양+MG-132조적조망지수요저우고양조,차이유현저성(P<0.05).고양+MG-132조Bcl-2/Bax치(1.22±0.15)고우고양조(0.87±0.11),차이유현저성(P<0.05).결론 고양유발폐조직세포발생조망,단백매체억제제MG-132가이통과조절Bcl-2여Bax적표체감경고양인기적세포조망.
Objective To observe the effect of the proteasome inhibitor MG-132 on pulmonary epithelial cell apoptosis in rats with hyperoxia-induced lung injury and to investigate the underlying mechanism. Methods Completely randomized design was adopted for this study. Twenty-six SD rats were randomly divided into 4 groups :hyperoxia group (n=8), hyperoxia plus MG-132 group (n=8), MG-132 group (n=5) ,control group (n =5). Based on the hyperoxia-induced lung injury rat model,the following parameters were determined: histopathological changes of lung tissue, cell apoptosis index via TUNEL method, Bax and Bcl-2 expression via immunohistochemistry. Additionally, Bcl-2/Bax ratio was calculated. Results After hyperoxia exposure,serious acute inflammatory reaction was found in hyperoxia group. The apoptosis index of hyperoxia group and hyperoxia plus MG-132 group (66.76±7.64,34.78±4.40 ) were significantly higher than those of control group and MG-132 group (14.48±1.75,12.88±1.95), and furthermore, hyperoxia plus MG132 group had lower apoptosis index than hyperoxia group (1.22±0.15 vs. 0.87±0.11, P<0.05). Hyperoxia plus MG-132 group had higher Bcl-2/Bax ratio than hyperoxia group (P<0.05). Conclusion Hyperoxia can induce pulmonary epithelial cell apoptosis. Proteasome inhibitor MG-132 can alleviate hyperoxia-induced lung injury through regulating Bax and Bcl-2 expression.
