蕨麻多糖对大鼠脑缺血再灌注损伤的保护作用及其机制

目的 探讨蕨麻多糖（PAP）对大鼠脑缺血再灌注损伤的保护作用及其机制.方法 将Wistar 雄性大鼠120只,随机分为6组：假手术组、模型组、尼莫地平组（12 mg/kg）和蕨麻多糖高[160 mg/（kg·d）]、中[80 mg/（kg·d）]、低[40 mg/（kg·d）]剂量组.采用线栓法栓塞大鼠大脑中动脉建立大鼠脑缺血再灌注损伤模型,从术前7d开始,每天1次,再灌注后1h给药1次.再灌注结束后进行神经功能缺失症状评分;分别用化学比色法测定脑组织超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和丙二醛（MDA）含量;酶联免疫吸附法（ELISA）测定肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-10（IL-10）含量.结果 与假手术组比较,模型组大鼠神经功能缺失症状明显,模型组大鼠脑组织SOD、GSH-Px、IL-10含量明显降低,MDA、TNF-α、IL-1β含量显著升高（P＜0.05）;与模型组比较,蕨麻多糖各剂量组大鼠神经功能缺失症状明显改善,蕨麻多糖能降低脑组织MDA、TNF-α和IL-1β含量,升高SOD、GSH-Px和IL-10含量（P＜0.05）;并且这种影响与蕨麻多糖剂量存在对应关系.结论 蕨麻多糖对大鼠脑缺血再灌注损伤具有一定保护作用,其机制可能与其提高脑组织抗氧化能力、抑制炎症因子有关.

The Protective Effect and Mechanism of Potentilla Anserine Polysaccharide on Cerebral Ischemic Injury of Rats

Objective To investigate the protective effect and mechanism of Potentilla anserine polysaccharide（ PAP） on the rat model of cerebral ischemia- reperfusion injury. Methods 120 Wistar male rats were randomly divided into 6 groups： sham operation group,model control group,Nimodipine group（ 12 mg / kg） and high dose group（ 160 mg·kg^- 1·d^- 1）,middle dose group（ 80 mg·kg^- 1·d^- 1）,low dose group（ 40 mg·kg- 1· d^- 1） dose of PAP group. The model of cerebral ischemia- reperfusion injury was established by inserting a nylon thread into the middle cerebral artery and then practiced administration,respectively once a day for seven days before the surgery,1 hour before reperfusion. Neurological deficits score was conducted at the end of reperfusion. Finally,the activity of brain tissue superoxide dismutase（ SOD）,content of glutathione peroxidase（ GSH- Px） and malondialdehyde（ MDA） by means of chemical colorimetry were measured; the contents of tumor necrosis factor-α（ TNF- α）,interleukin- 1β（ IL- 1β） and interleukin- 10（ IL- 10） of the brain were essayed by enzyme linked immunosorbent assay（ ELISA）. Results Compared with sham operation group,neurological deficits of rats were improved significantly in model group. The activity of SOD,GSH- Px and IL- 10 of model control group rats decreased apparently,while the contents of MDA,TNF- α,IL- 1β（ P〈0. 05） in the brains increased remakably（ P〈0. 05）; compared with model group,neurological deficits of rats were improved significantly in each PAP dose groups. PAP could significantly decrease the contents of MDA,TNF- α,IL- 1β,and remarkably increased the activity of SOD,GSH- Px and IL- 10（ P〈0. 05）. And there is a correspondence between the impact and dose of PAP. Conclusion PAP have a protective effect on cerebral ischemia- reperfusion injury,and its mechanism may be by improving antioxidant capacity and inhibit inflammation initial factor to protective of cerebral ischemia-reperfusion injury.