目的 探讨大麻素1(CB1)受体拮抗剂利莫那班对大鼠局灶性脑缺血/再灌注损伤的保护作用.方法 线栓法制备大鼠局灶性脑缺血/再灌注模型.36只雄性大鼠随机分为假手术组、手术组、尼莫地平对照组、利莫那班低剂量组、中剂量组和高剂量组.再灌注24 h后进行神经功能评分(NFS),TTC染色测定梗死面积,HE染色检测脑组织病理变化,免疫组化染色观察P-erk1/2和caspase-3免疫阳性表达,并检测大鼠脑组织匀浆中超氧化物歧化酶(SOD)和丙二醛(MDA)变化.结果 利莫那班能明显改善大鼠的神经行为,缩小梗死面积,并使脑组织病理改变减轻,SOD活性明显升高,MDA含量明显降低,下调caspase-3的表达,上调P-erk1/2的表达.结论 利莫那班对局灶性脑缺血/再灌注大鼠有明显的保护作用,其机制可能与拮抗大麻素受体、抑制细胞凋亡有关.%Objective To investigate the protective effects of rimonabant on cerebral ischemia reperfusion (CIR) injury in rats.Methods The CIR model was built through thread block. 36 male rats were randomly divided into sham operation, operation, nimodipine,low, middle and high dose rimonabant groups. 24 h later, the neurologic deficit score and infarction area were measured. Then pathological change in injury brain tissue was detected by HE stain. The caspase-3 and P-erk protein expressions were detected by immunohistochemistry. At the same time,the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in brain tissue were observed. Results Rimonabant reduced cerebral infarction area, and relieved the injury of brain tissue. It increased the activity of SOD and decreased the contents of MDA. It also reduced the expression of caspase-3, and increased the expression of P-erk. Conclusions Rimonabant has an obviously neuroprotective effect on ischemic cellular injury by antagonising CB1. The Neuronal apoptosis may be involved in the protective mechanism.
展开▼
