摘要
目的研究原花青素(GSP)对大鼠局灶性脑缺血再灌注损伤抗炎作用机制。方法大鼠脑缺血再灌注模型完成后,缺血2h再灌注24h,其中原花青素大剂量组(40mg/kg)、小剂量组(10mg/kg)术前7d分别腹腔注射2ml/kgGSP,模型组腹腔注射2ml/kg生理盐水,1次/d,再灌注前15min加注1次。观察不同剂量的原花青素对脑组织一氧化氮(NO)含量、髓过氧化物酶(MPO)活性和脑组织神经细胞的细胞间黏附分子-1(ICAM-1)蛋白的表达的影响。结果原花青素可显著减轻大鼠脑缺血再灌注损伤的行为评分;显著降低脑组织中NO含量和MPO的活性,差异有统计学意义(P<0.05);ICAM-1蛋白的阳性表达率降低,差异有统计学意义(P<0.05)。结论原花青素对大鼠脑缺血再灌注损伤有保护作用,作用机制之一可能与其抑制炎性反应有关。
Objective To investigate the Anti-Inflammatory mechanisms of grape seed procyanidin （GSP） on cerebral ischemia reperfusion injury （CIRI） of rats. Methods The model of MCAO was established by intraluminal suture technique. After 2 h of occlusion and 24 h of reperfusion ,The high dose GSP （40 mg/kg） group and low dose GSP （ 10 mg/kg） group, was injected by intraperitoneal injection for 7 days ,and all groups were given a more time in 15 minutes before operation. The contents of NO and activities of MPO in brain tissue of ischemic hemisphere were measured; the expression of ICAM-1 in the cortex were measured by immunohistochemical method. Results The neurological scores of rats treated with GSP was reduced apparently compared with model group rats （ P 〈 0.05 ） ; there were apparent reduction of the contents of NO and marked decrease of MPO in GSP group compared with the I/R model group （ P 〈 0. 05 ） ; compared with/JR model group, the expression of ICAM-1 was down-regulated obviously in GSP group （P 〈 0. 05 ）. Conclusion GSP could reheve the cerebral ischemia reperfusion injury, one of the mechanisms could be the Anti-Inflammatory effect of procyanidin
出处
《中国实用医药》
2009年第2期12-13,共2页
China Practical Medicine
