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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 investigate the changes of ICAM-1 gene expression in rat brain after + GZ repeated exposure and to explore the molecular mechanism of + GZ-induced brain injury. Methods: Twenty four Sprague Dawley rats were randomly divided into four groups: control group (30 min, 6 h and 24 h), and 6 rats in each group. Rats in the experimental group experienced three times +10 GZ / 3 minutes (two intervals of 30 minutes) on the animal centrifuge, and the G value of the control group was + 1GZ. The rats were sacrificed at 30 min, 6 h and 24 h after exposure respectively. The total RNA was extracted and the expression of ICAM was detected by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) - 1m R-NA expression level. Results: The levels of ICAM-1mRNA in brain tissue of rats exposed to + GZ for 30 min, 6 h and 24 h were 1.7, 3.0 and 1.9 times higher than that of the control group respectively. CONCLUSION: Repeated exposure of + GZ can induce the expression of ICAM-1mRNA in rat brain and mediate the enhanced adhesion of leucocytes and brain microvascular endothelial cells, which play a role in the pathological process of brain damage induced by + GZ.