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目的探讨阿司匹林对脑缺血再灌注损伤炎症反应的影响及其机制。方法采用线栓法制备短暂性大脑中动脉缺血模型,用免疫组织化学染色观察脑组织中核转录因子-κB(NF-κB)活性、白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)的表达;HE染色观察中性粒细胞浸润。结果与对照组比较,小剂量阿司匹林组和大剂量阿司匹林组的NF-κB活性降低,以大剂量的阿司匹林作用更为明显;各阿司匹林组的IL-1β、TNF-α的表达明显降低,白细胞浸润明显减少。结论阿司匹林可抑制脑缺血再灌注损伤过程中的炎症反应;其机制可能与抑制NF-κB的激活和IL-1β、TNF-α表达有关。
Objective To investigate the effect and mechanism of aspirin on inflammatory reaction after cerebral ischemia-reperfusion injury. Methods The model of transient middle cerebral artery occlusion (MCAO) was established by thread occlusion. The expression of NF-κB, IL-1β, TNF- α (TNF-α) expression; HE staining observed neutrophil infiltration. Results Compared with the control group, the activity of NF-κB in low-dose aspirin group and high-dose aspirin group was decreased, especially in high-dose aspirin group. The expressions of IL-1β and TNF-α in each aspirin group were significantly decreased, obviously decrease. Conclusion Aspirin can inhibit the inflammatory reaction during the process of cerebral ischemia-reperfusion injury. Its mechanism may be related to the inhibition of the activation of NF-κB and the expression of IL-1β and TNF-α.