摘要
目的 :了解 +GZ重复暴露后大鼠脑组织细胞间粘附因子 - 1(ICAM- 1)基因表达的变化 ,探讨 +GZ引起脑损伤的分子机制。 方法 :2 4只 SD大鼠随机分成对照组、+GZ重复暴露后 30 min、6 h和 2 4h四组 ,每组 6只。实验组大鼠在动物离心机上经历了 3次 +10 GZ/ 3min(两次中间间隔 30 min)作用 ,对照组大鼠 G值为 +1GZ。分别于暴露后 30 min、6 h和 2 4h处死大鼠取脑 ,提取总 RNA,用半定量反转录聚合酶链反应 (RT- PCR)检测方法检测 +GZ重复暴露后大鼠脑组织 ICAM- 1m R-NA表达水平。 结果 :+GZ重复暴露后 30 min、6 h和 2 4h大鼠脑组织 ICAM- 1m RNA均明显升高 ,分别是对照组的 1.7倍、3.0倍和 1.9倍。 结论 :+GZ重复暴露可诱导大鼠脑组织 ICAM- 1m RNA的表达 ,介导了白细胞、脑微血管内皮细胞的粘附增强 ,在 +GZ所致脑损害的病理过程中起一定作用。
Objective To study the changes of mRNA expression of intercellular adhesion molecule 1(ICAM 1) in the brain of rat exposured to repeated +G Z, and to explore the molecular mechanism of brain damage induced by repeated +G Z exposures. Methods Twenty four concious SD rats served as subjects, using an animal centrifuge, control rats ( n =6) were exposed to +1G Z and experimental rats ( n =18) were exposed to +10G Z three times, each for 3 min with 30 min interval in between. The brains were taken 30 min, 6h and 24h after the last centrifuge run and total RNA was isolated. The mRNA expression levels of ICAM 1 in rat brain exposured to repeated +G Z were measured by semi quantitative reverse transcription polymerase chain reaction (RT PCR). Results The ICAM 1 mRNA expression levels in rat brains taken 30 min, 6h and 24h after repeated +G Z exposures were significantly higher than those of control group. Conclusion It is suggested that ICAM 1 mRNA expression in rat brain can be inducted by repeated +G Z exposures and the increased ICAM 1 mRNA expression may play a role in the pathologic course of brain damage induced by+G Z exposures.
出处
《空军总医院学报》
2000年第2期63-65,共3页
Journal of General Hospital of Air Force,PLA
基金
全军医药卫生科研基金!课题 ( 98D0 3 3 )
空军后勤部科研基金