大鼠严重创伤后早期下丘脑CRH的表达

目的 探讨在颅脑撞击伤应激反应中下丘脑表达和分泌促肾上腺皮质激素释放激素（CRH）的变化规律及其反馈调节机制。方法 应用BIM－Ⅲ型多功能小型生物撞击机致伤，采用免疫组化和Western blot等技术进行检测下丘脑CRH的表达变化和分布规律。分组：对照组、撞击伤后15min、30min、1h、2h、6h、12h撞击伤组、撞击伤治疗组，治疗组用CRH1受体（CRH1R）特异性阻滞剂CP－154526处理。结果 正常情况下，CRH少量的表达于下丘脑室旁核和视上核，撞击伤后1h CRH表达明显增加，主要分布于室旁核和视上核，且表达呈逐渐增加的趋势，在2－6h时相点表达明显增加，6h后开始回落；用CP－154526治疗的大鼠，撞击伤后下丘脑CRH表达的增加明显减少。结论 在创伤性应激反应中，CRH对下丘脑合成和分泌CRH存在明显的调节作用，CRH通过与CRH1R的结合在其中可能起着关键的作用。

Effect of severe traumatic injury on the expression of corticotropin releasing hormone in the hypothalamus in rats

Objective To investigate the function and expression of corticotropin releasing hormone(CRH) in the hypothalamus in rats following severe traumatic lung injury. Methods Rats were traumatized by using BIM III Multifunctional Biological Impactor and then divided into control, 15 min, 30 min, 1 h, 2 h, 6 h, 12 h post trauma groups and treated group. Rats were deeply anesthetized and sacrificed at 15 min, 30 min, 60 min, 120 min, 360 min and 720 min after traumatic lung and right femora cataclasis injury. The changes of expression and concentrations of CRH in the hypothalamus in rats were detected by immunocytochemistry and Western blot. CRH 1R specific blocker CP 154526 was used in treated group. Results CRH was present in the hypothalamic paraventricular nucleus(PVN) and supraoptic nucleus(SON). In response to severe traumatic lung injury onset, a significant increase in CRH mRNA level was noted at 120 min after trauma, and then gradually increased to the peak at 720 min after trauma. CP 154526 could significantly inhibit the expression of CRH. Conclusion In response to traumatic stress, CRH from the PVN and SON are involved in the control of the synthesis and release of CRH from hypothalamus after severe traumatic lung injury, suggesting that CRH may play an important role through the combination with CRH type 1 receptor.