【摘要】：目的檢測創(chuàng)傷后應(yīng)激障礙(post traumatic stress disorder,PTSD)大鼠海馬區(qū)環(huán)氧合酶-2(cyclooxygenase-2,COX-2)水平和應(yīng)用COX-2抑制劑塞來昔布(celecoxib)后對大鼠神經(jīng)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為正常對照組、PTSD組、COX-2抑制劑治療組,通過曠場實驗、高架十字迷宮實驗、水迷宮實驗評估大鼠行為能力;通過免疫組織化學(xué)染色、RT-PCR與Western blot測量大鼠海馬組織COX-2表達情況;ELISA法檢測大鼠海馬組織白介素-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;應(yīng)用Griess法檢測海馬組織一氧化氮(nitric oxide,NO)的表達。結(jié)果 RT-PCR及Western blot檢測顯示,治療組COX-2mRNA及蛋白表達低于模型組而高于正常對照組,差異有統(tǒng)計學(xué)意義(均P0.05),ELISA檢測顯示治療組IL-1、IL-6、PEG2含量低于模型組而高于正常對照組,差異有統(tǒng)計學(xué)意義(均P0.05),Griess法檢測治療組NO含量低于模型組而高于正常對照組,差異有統(tǒng)計學(xué)意義(均P0.05),且治療組較模型組行為學(xué)功能得到改善。結(jié)論 PTSD大鼠海馬中IL-1、IL-6及COX-2的水平升高,同時其下游NO、PGE2的表達增加,推測COX-2是PTSD致病機制中的重要環(huán)節(jié),COX-2抑制劑可能通過抑制炎性因子表達改善PTSD大鼠神經(jīng)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.
【作者單位】： 武漢市第一醫(yī)院神經(jīng)外科;
【基金】：湖北省自然科學(xué)基金資助項目(No.2015CFB694) 武漢市衛(wèi)生計生委資助項目(No.WZ16C10)
【分類號】：R749.5

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