中文摘要：

目的 探讨西洋参茎叶皂苷对脑缺血再灌注损伤大鼠脑组织一氧化氮（NO）和一氧化氮合酶（NOS）表达的影响及其相关机制。方法 SD大鼠50只,随机分为假手术组、模型组、西洋参茎叶皂苷（50、100、200 mg·kg^-1）组5组,采用线栓法制备大鼠脑缺血再灌注损伤模型。造模前,西洋参茎叶皂苷治疗组分别灌胃给药,每日1次,连续7 d。脑缺血再灌注24h后以Longa＇s法进行大鼠神经功能损伤评分,分光光度计法检测脑组织中一氧化氮（NO）含量及一氧化氮合酶（NOS）、诱导型一氧化氮合酶（i NOS）活性。结果 与模型组比较,西洋参茎叶皂苷（100、200 mg·kg^-1）组可明显改善大鼠脑缺血再灌注后神经功能损伤（1.80±0.68 vs.2.30±0.51,P〈0.05;1.50±0.76 vs.2.30±0.51;P〈0.05）,降低缺血脑组织NOS和i NOS的活性（3.82±0.41 vs.5.83±0.68,P〈0.05;3.13±0.38 vs.5.83±0.68,P〈0.01;1.49±0.9 vs.1.93±0.11,P〈0.05;1.13±0.8 vs.1.93±0.11,P〈0.01）,进而减少NO的生成（30.11±3.91 vs.46.73±5.58,P〈0.01;27.18±3.38 vs.46.73±5.58,P〈0.01）。结论 西洋参茎叶皂苷对大鼠脑缺血再灌注损伤具有保护作用,其机制可能与其抑制NOS和i NOS表达而使NO含量降低,进而减轻大脑神经功能损伤有关。

英文摘要：

Objective To investigate the effect of Panax quinquefolium saponins from steams and leaves （PQS）on the expression of NO and NOS in rats with cerebral ischemic reperfusion injury and study its mechanism. Methods The SD rats were randomly divided into sham operation group, cerebral ischemiareperfusion model group, PQS（50,100,200mg·kg^-1） group. Cerebral ischemia reperfusion model was established with suture emboli method in middle cerebral artery of rats. The rats in PQS treatment groups were treated with PQS once a day for 7 days before the surgery. Neurological deficit scores were measured by Longas method 24 hours after the cerebral reperfusion. The nitric oxide （NO） content,the activity of nitric oxide synthase （NOS） and inducible NOS （iNOS） in the brain tissues were determined with the method of spectrophotometry. Results Neurological deficit scores （ 1.80 ± 0.68 vs. 2.30± 0. 51 ,P 〈0.05 ;1.50 ±0.76 vs. 2.30 ±0.51 ;P 〈0.05）, the activity of NOS and iNOS（3.82 ±0.41 vs. 5.83 ±0.68 ,P 〈0.05 ;3.1±0.38 vs. 5.83±0.68,P〈0.01;1.49±0.9 vs. 1.93±0.11,P〈0.05;1.13±0.8 vs. 1.93±0.11,P〈0.01）, and NO content （ 30.11 ± 3.91 vs. 46.73 ±5.58,P 〈 0.01 ;27.18 ±3.38 vs. 46.73 ±5.58,P 〈 0.01 ） were significantly decreased in PQS （ 100,200mg·kg^-1 ） groups than ischemia - reperfusion model group. Conclusion PQS exerts the neuroprotective effect on cerebral ischemia - reperfusion injury in rats. The mechanism may be associated with reducing the content of NO and the activiy of NOS dose - dependently.