MC-002对脑缺血再灌注损伤大鼠脑组织及血清中NO及NOS的影响

目的 研究MC-002对脑缺血再灌注损伤大鼠脑组织及血清中一氧化氮（NO）、一氧化氮合酶（NOS）含量的影响,探讨其对脑缺血再灌注损伤保护作用的机制.方法 采用改良线栓法,建立大鼠大脑中动脉栓塞（MCAO）脑缺血再灌注模型.将雄性SD大鼠随机分为假手术组、模型组、奥扎格雷钠组（18mg/kg）和MC-002高、中、低剂量组（30、18、10.8mg/kg）.缺血再灌注24h后检测脑组织及血清中NO含量、NOS活性.结果 与假手术组相比,模型组脑组织和血清中NO含量和NOS活性明显升高;与模型组相比,MC-002高、中、低剂量组脑组织和血清中NO含量和NOS活性均明显降低（P＜0.01、0.05）.结论 MC-002对大鼠脑缺血再灌注损伤具有明显的保护作用,其机制可能与降低NOS活性,减少NO含量有关.

Effect of MC 002 on the NO and NOS in serum and brain tissue of rats with cerebral ischemia-reperfusion injury

Objective To observe the effect of MC-002 on the contents of NO and NOS in serum and brain tissue of rats with cerebral isehemia-reperfusion injury and investigate the protective effect mechanism of MC 002. Methods Rat model of cerebral ischemia-reperfusion injury was created by the middle cerebral artery occlusion （MCAO） by modified suture meth- od. Healthy male SD rats were randomly divided into six group： Sham-operated group, model group, sodium ozagrel group （18mg/kg） ,and high-, middle-, and low-dose （30,18, and 10.8mg/kg） of MC 002 groups. After being established by the MCAO method,the NO and the NOS of rats were detected after the ischemia-reperfusion for 24h. Results Compared with the sham operation group, the NO level and NOS activity of model group were higher significantly. The NO level and the NOS activ- ity were decreased obviously in the MC 002 group when they comparing with the model group （P 〈 0.01,0.05 ）. Condusion MC-002 shows protective effects on cerebral ischemia-reperfusion injury. The mechanism may be ralated to refrain the ex- pression of NO and NOS.