帕瑞昔布钠对老年大鼠术后认知功能的影响-东南大学学报医学版

帕瑞昔布钠对老年大鼠术后认知功能的影响

单位：1. 四川省人民医院, 麻醉科, 四川成都 610000;
2. 四川省人民医院, 疼痛科, 四川成都 610000

分类号：R614

出版年·卷·期（页码）：2019·38·第一期（19-22）

摘要：

目的：探讨帕瑞昔布钠对老年大鼠术后认知功能障碍（POCD）的影响及可能的作用机制。方法：100只老年SD大鼠，随机分为对照组、模型组、治疗组，模型组和治疗组大鼠采用腹腔探查术制备POCD模型后，治疗组给予5 mg·kg^-1帕瑞昔布钠治疗，模型组给予等体积生理盐水。采用Morris水迷宫评价各组大鼠学习认知能力；采用免疫组化法测定海马星形胶质细胞活化情况；采用酶联免疫吸附法（ELISA）检测大鼠海马区中IL-1β、IL-6、TNF-α表达；Western blotting测定各组大鼠海马COX-2、iNOS蛋白表达。结果：与模型组大鼠比较，治疗组大鼠Morris水迷宫的逃避逃避潜伏期显著下降（P<0.05），穿越平台次数显著增加（P<0.05）；与模型组比较，治疗组大鼠海马区海马星形胶质细胞平均光密度值、IL-1β、IL-6、TNF-α、COX-2、iNOS水平显著下降（P<0.05）。结论：帕瑞昔布钠能通过抑制COX-2，降低海马区中IL-1β、IL-6、TNF-α的表达，降低iNOS的表达对老年大鼠POCD起到保护作用。

Objective:To investigate the effect of parecoxib on postoperative cognitive dysfunction of geriatric rats and the possible mechanism. Methods:One hundred geriatric SD rats were randomly divided into control group, model group, treatment group. Abbreviated laparotomy was used by rats in the model group and the treatment group to build postoperative cognitive dysfunction (POCD) model. The rats in the treatment group were administrated 5 mg·kg^-1 parecoxib and rats in the model group were administrated saline (the same volume as the treatment group). Morris water maze was performed to evaluate the learning cognition of rats. Immunohistochemistry was performed to determine the activation of hippocampal astrocytes. Enzyme-linked immunosorbent assay (ELISA) was used to determine the expression of IL-1β, IL-6 and TNF-α in the hippocampus of rats. Western blot was used to determine the expression of COX-2 and iNOS in the hippocampal of rats. Results:Compared with the model group, the avoidance latency of Morris water maze in the treatment group was significantly decreased while the number of crossings was significantly increased (P<0.05). Compared with the model group, average optical density of astrocyte, IL-1β, IL-6, TNF-α, COX-2, iNOS in hippocampusin were significantly decreased in the hippocampus region of the treatment group (P<0.05). Conclusion:Paracoxib can protect the postoperative cognitive dysfunction of geriatric rats by inhibiting of COX-2, decreasing expression of IL-1β, IL-6, TNF-α in the hippocampus, reducing the expression of iNOS.

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