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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 study the anti-inflammatory mechanism of proanthocyanidins (GSP) on focal cerebral ischemia-reperfusion injury in rats. Methods After cerebral ischemia-reperfusion model was established, ischemia-reperfusion was performed for 2 hours and 2 hours after reperfusion, in which the proanthocyanidin high dose group (40mg / kg) and the low dose group (10mg / kg) Intraperitoneal injection of 2ml / kg saline, 1 / d, 15min before reperfusion filling 1. To observe the effects of different doses of proanthocyanidins on the content of nitric oxide (NO), the activity of myeloperoxidase (MPO) and the expression of intercellular adhesion molecule-1 (ICAM-1) in brain tissue. Results Proanthocyanidins significantly reduced the behavioral scores of rats with cerebral ischemia-reperfusion injury and significantly decreased NO content and MPO activity in brain tissue (P <0.05). The positive rate of ICAM-1 protein was decreased, The difference was statistically significant (P <0.05). Conclusion Proanthocyanidins have a protective effect on cerebral ischemia-reperfusion injury in rats, and one of the mechanisms may be related to its inhibition of inflammatory reaction.