美洛昔康对全脑缺血/再灌注大鼠脑损伤的作用观察

目的探讨美洛昔康对大鼠全脑缺血/再灌注损伤的保护作用。方法采用双侧颈总动脉夹闭合并低血压方法建立全脑缺血/再灌注大鼠模型。美洛昔康(1、3和5mg·kg-1)在缺血前30min腹腔注射给药。Morris水迷宫测定大鼠空间学习能力,病理切片HE染色观察海马神经元形态结构,免疫组化检测海马组织核转录因子NF-κB p65蛋白表达,生物酶学方法观察超氧歧化酶活性和丙二醛含量。结果美洛昔康能明显缩短全脑缺血/再灌注大鼠的寻台潜伏期,减轻全脑缺血/再灌注大鼠海马神经元损伤,降低海马神经元NF-κB p65蛋白表达,明显阻遏全脑缺血/再灌注大鼠海马MDA含量的升高和SOD活性的降低。结论美洛昔康对全脑缺血/再灌注致大鼠脑损伤有明显的保护作用,其机制可能与其抑制COX-2活性,减少PGs等代谢产物的产生,抑制NF-κB活性,从而抑制炎症反应和氧化应激功能有关。

Effect of meloxicam on global cerebral ischemia reperfusion injury in rats

Aim To investigate the effect of meloxicam on global cerebral ischemia reperfusion(IR) injury in rats.Methods The rat model of global cerebral ische-mia reperfusion injury was established by bilateral common carotid arteries occlusion combined with hemorrhagic hypotension.Meloxicam (1,3 and 5mg·kg-1) was intraperitoneally administered 30 min before the operation.Morris water maze was used to evaluate the ability of spatial learning and memory function.HE staining was used to observe pathomorphological changes of hippocampal neurons.NF-κB p65 expression was detected by immunohistochemistry,SOD activities and MDA contents were analyzed by biochemical method.Results Meloxicam remarkably improved the spatial learning and memory function,obviously prevented the hippocampal neurons from karyopycnosis induced by IR.Meloxicam significantly blunted the increase of MDA content,NF-κB p65 protein expression,and the decrease of SOD activities in IR rats.Conclusions Meloxicam has a obvious neuroprotective effect on global cerebral ischemia reperfusion damage.The anti-inflammation and antioxidative stress of meloxicam may be involved in the protective mechanism.