环氧合酶-2抑制剂对创伤后应激障碍大鼠神经功能的改善

发布时间：2019-03-07 13:39

【摘要】：目的检测创伤后应激障碍(post traumatic stress disorder,PTSD)大鼠海马区环氧合酶-2(cyclooxygenase-2,COX-2)水平和应用COX-2抑制剂塞来昔布(celecoxib)后对大鼠神经功能的改善作用,研究COX-2在PTSD中的可能作用。方法成年雄性大鼠分为正常对照组、PTSD组、COX-2抑制剂治疗组,通过旷场实验、高架十字迷宫实验、水迷宫实验评估大鼠行为能力;通过免疫组织化学染色、RT-PCR与Western blot测量大鼠海马组织COX-2表达情况;ELISA法检测大鼠海马组织白介素-1(interleukin-1,IL-1)、白介素-6(interleukin-6,IL-6)以及前列腺素E2(prostaglandin E2,PGE2)的水平;应用Griess法检测海马组织一氧化氮(nitric oxide,NO)的表达。结果 RT-PCR及Western blot检测显示,治疗组COX-2mRNA及蛋白表达低于模型组而高于正常对照组,差异有统计学意义(均P0.05),ELISA检测显示治疗组IL-1、IL-6、PEG2含量低于模型组而高于正常对照组,差异有统计学意义(均P0.05),Griess法检测治疗组NO含量低于模型组而高于正常对照组,差异有统计学意义(均P0.05),且治疗组较模型组行为学功能得到改善。结论 PTSD大鼠海马中IL-1、IL-6及COX-2的水平升高,同时其下游NO、PGE2的表达增加,推测COX-2是PTSD致病机制中的重要环节,COX-2抑制剂可能通过抑制炎性因子表达改善PTSD大鼠神经功能。
[Abstract]:Objective to detect the level of cyclooxygenase-2 (cyclooxygenase-2,COX-2) in hippocampus of rats with post-traumatic stress disorder (post traumatic stress disorder,PTSD) and the effect of COX-2 inhibitor celecoxib (celecoxib) on neurologic function in rats. The possible role of COX-2 in PTSD was studied. Methods Adult male rats were divided into three groups: normal control group, PTSD group and COX-2 inhibitor treatment group. The behavior ability of rats was evaluated by open field test, elevated maze test and water maze test. The expression of COX-2 in hippocampus of rats was measured by immunohistochemical staining with RT-PCR and Western blot. The levels of interleukin-1 (interleukin-1,IL-1), interleukin-6 (interleukin-6,IL-6) and prostaglandin E _ 2 (prostaglandin E _ 2, PGE _ 2) in hippocampus of rats were measured by ELISA. The expression of nitric oxide (nitric oxide,NO) in hippocampus was detected by Griess method. Results RT-PCR and Western blot showed that the expression of COX-2mRNA and protein in the treatment group was lower than that in the model group, but higher than that in the normal control group. The difference was statistically significant (P0.05), ELISA test showed IL-1,IL-6, in the treatment group). The content of PEG2 in the treatment group was significantly lower than that in the model group but higher than that in the normal control group (P 0.05). The NO content in the treatment group was significantly lower than that in the model group but higher than that in the control group (all P0.05). The behavioral function of the treatment group was improved than that of the model group. Conclusion the levels of IL-1,IL-6 and COX-2 in hippocampus of PTSD rats are increased, and the expression of downstream NO,PGE2 is also increased. It is suggested that COX-2 is an important link in the pathogenesis of PTSD. COX-2 inhibitor may improve the nerve function of PTSD rats by inhibiting the expression of inflammatory factors.
【作者单位】：武汉市第一医院神经外科;
【基金】：湖北省自然科学基金资助项目(No.2015CFB694) 武汉市卫生计生委资助项目(No.WZ16C10)
【分类号】：R749.5

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