论文部分内容阅读
目的:探讨三七总皂苷(PNS)对缺血再灌注损伤后大鼠大脑皮层组织丙二醛(MDA)的含量、谷胱甘肽过氧化物酶(GSH-PX)的活性的影响。方法:采用线栓法制备大鼠大脑中动脉局灶缺血再灌注模型,选用Wistar雄性大鼠(54只)随机分成3组,即:假手术组(12只)、缺血再灌注组(24只)、三七总皂苷治疗组(18只);再根据灌注时间不同分为再灌注10h、12h、24h组,每组是8只。缺血时间为90min。各组动物给药方法:三七总皂苷治疗组(PNS组)腹腔注射1%PNS(50mg/kg),每天一次,持续10天;假手术组和缺血再灌注模型组腹腔注射与PNS组等体积的生理盐水10天,各组于术前1h再注射1次。进行HE染色观察脑皮层组织形态病理学变化;硫代巴比妥酸比色法检测MDA的含量;二硫双硝基苯甲酸法检测GSH-PX的活性。结果:缺血再灌注组GSH-PX的活性降低(P<0.05),MDA的含量升高(P<0.05);PNS治疗组GSH-PX的活性明显增强(P<0.05),MDA的含量明显下降(P<0.05)。结论:PNS可能通过增加GSH-PX的活性和减少MDA的含量来拮抗缺血再灌注损伤后脑组织的脂质过氧化,发挥脑组织的保护作用。
Objective: To investigate the effect of Panax Notoginseng Saponins (PNS) on the content of malondialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) in rat cerebral cortex after ischemia-reperfusion injury. Methods: The focal middle cerebral artery occlusion (MCAO) model of rat middle cerebral artery was prepared by thread plug method. Fifty-four Wistar male rats were randomly divided into three groups: sham operation group (12 rats), ischemia reperfusion group 24), Panax notoginseng group (18), and then divided into reperfusion 10h, 12h, 24h group according to different perfusion time, each group is 8. Ischemic time was 90min. Each group of animals were dosed: PNS group (PNS group) intraperitoneal injection of 1% PNS (50mg / kg) once a day for 10 days; sham operation group and ischemia-reperfusion model group, intraperitoneal injection and PNS group The same volume of saline for 10 days, each group 1h before surgery and then injected once. The morphological changes of cerebral cortex were observed by HE staining. The content of MDA was detected by thiobarbituric acid colorimetric assay. The activity of GSH-PX was detected by dithiobisnitrobenzoate method. Results: The activity of GSH-PX was decreased (P <0.05) and the content of MDA was increased in ischemia-reperfusion group (P <0.05). The activity of GSH-PX in PNS group was significantly increased Decreased (P <0.05). CONCLUSION: PNS may antagonize the lipid peroxidation of brain tissue after ischemia-reperfusion injury by increasing the activity of GSH-PX and decreasing the content of MDA, and exert the protective effect of brain tissue.