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目的探讨乌司他丁(UTI)对大鼠脑缺血再灌注后认知记忆功能、核因子-κB(NF-κB)的表达、炎症因子及氧化介质改变的影响。方法线栓法制备大鼠局灶性脑缺血再灌注损伤模型。于脑缺血2 h再灌注24 h后,采用组织病理学法观察海马区形态学变化;Western blot和图像分析技术检测海马NF-κB p65的表达;酶联免疫检测法(ElISA)测定肿瘤坏死因子(TNF-α)、白细胞介素-10(IL-10)的含量;生物化学比色法测定超氧化物歧化酶(SOD)、脂过氧化产物丙二醛(MDA)的水平。另取大鼠进行Morris水迷宫测试。结果 UTI提高海马区存活锥体细胞数,改善组织病理变化;可显著增强大鼠海马NF-κB的表达;明显降低致炎因子TNF-α的水平,升高抗炎因子IL-10的水平;降低MDA的含量,升高抗氧化介质SOD的含量;使逃避潜伏期缩短,平台象限距离百分比增加,穿越平台次数增加。结论 UTI能增强脑缺血再灌注损伤大鼠认知记忆能力,抗炎及抗氧化作用是其可能机制。
Objective To investigate the effect of ulinastatin (UTI) on cognitive memory function, expression of NF-κB, inflammatory factors and oxidative mediators after cerebral ischemia-reperfusion in rats. Methods The rat model of focal cerebral ischemia / reperfusion injury was established by suture method. Histological changes in the hippocampus were observed by histopathology at 2 h after reperfusion for 2 h. Western blot and image analysis were used to detect the expression of NF-κB p65 in hippocampus. Elisa was used to detect tumor necrosis (TNF-α) and interleukin-10 (IL-10) were detected by spectrophotometry. The level of superoxide dismutase (SOD) and malondialdehyde (MDA) Another rat for Morris water maze test. Results UTI increased the number of viable pyramidal neurons in the hippocampus and the histopathological changes, increased the expression of NF-κB in the hippocampus, decreased the level of TNF-α, increased the level of anti-inflammatory cytokine IL-10 and decreased the level of MDA , Increased the content of SOD in antioxidative medium, shortened the escape latency, increased the distance from the platform quadrant and increased the number of crossing the platform. Conclusion UTI can enhance cognitive memory, anti-inflammatory and anti-oxidative effects of cerebral ischemia-reperfusion injury in rats is its possible mechanism.