尼美舒利对大鼠慢性脑缺血后白质损伤的改善作用

Neuroprotective effect of nimesulide on white matter damage after chronic cerebral hypoperfusion in the rat

目的:探讨诱导型环氧和酶(COX2)抑制剂尼美舒利对大鼠慢性脑缺血后白质损伤的改善作用。方法:36只SD大鼠随机分为对照组、缺血组和治疗组,后2组大鼠采用持久双侧颈总动脉结扎术造成慢性脑缺血及白质损伤模型。治疗组于术后24h以尼美舒利(6mg/kg)每d灌胃,对照组和缺血组以同等量的0.5g/L羧甲基纤维素钠灌胃,连续30d。各组于30d后做病理染色和免疫组化染色,观察脑组织病理学改变,胶质纤维酸性蛋白(GFAP)阳性细胞表达情况及β淀粉样前体蛋白(βAPP)阳性轴突表达情况。结果:与对照组相比,缺血组皮层下白质有神经纤维和髓鞘溃变,GFAP阳性细胞明显增多,βAPP免疫阳性轴突明显增多;治疗组以上变化明显减轻,且差异有统计学意义。结论:尼美舒利对慢性脑缺血后白质的损伤有改善作用。

Aim ： To investigate the neuroprotective effect of a cyclooxygenase-2 inhibitor, nimesulide, on white matter damage after chronic cerebral hypoperfusion in the rat, Methods： A total of 36 SD rats were allocated into sham operation group, chronic cerebral hypoperfusion group （CCH） and nimesulide treatment group randomly. The rats in the latter 2 groups were evoked white matter damage model by permanent bilateral occlusion of the common carotid arteries. The nimesulide treatment group received a daily oral dose of 6 mg/kg nimesulide from 24 h after the operation to 30 d,and the other 2 groups received control drugs. The histopathological changes of brain tissue, the positive expressions of GFAP and β-APP were examined using immunohistochemistry. Results： There were obvious white matter damage in the brain tissue of CCH rats and increase of β-APP immunopositive and GFAP positive cells. In nimesulide treatment group the damage were comparatively mild, Conclusion.The cyclooxygenase-2 inhibitor, nimesulide, has neuroprotective effects on the white matter damages induced by CCH in the rat,