摘要
目的:探讨人参二醇组皂苷(PDS)对失血性休克复合内毒素(LPS)二次打击大鼠肺组织氧化损伤的影响。方法:40只Wistar大鼠随机分为假手术对照组(S组)、失血-内毒素二次打击模型组(HL组)、地塞米松预治疗组(HLD)及PDS预治疗组(HLP组)。在失血性休克首次打击基础上,腹腔注入LPS作为第二次打击建立稳定急性肺损伤模型,用722S分光光度计测定大鼠肺组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量、一氧化氮合酶(NOS)活力、诱导型一氧化氮合酶(iNOS)活力和一氧化氮代谢产物(NO2-/NO3-)含量。结果:病理学观察显示,二次打击后肺组织出现了明显的炎症反应,且结构出现破坏,与HL组比较,HLD及HLP组炎症反应明显减轻。与S组比较,HL组SOD活力明显降低(P<0.01),NOS、iNOS活力及NO2-/NO3-、MDA含量显著增加(P<0.05或P<0.01);与HL组比较,HLP和HLD组肺组织SOD活力明显升高(P<0.01),而肺组织NOS、iNOS活力及NO2-/NO3-、MDA含量显著降低(P<0.05或P<0.01)。结论:氧化应激参与了二次打击急性肺损伤的发病过程,PDS可通过抗氧化损伤实现对肺脏的保护作用。
Objective To explore the effect of panaxadiols saponin (PDS) on the oxidative damage in lung tissue in hemorrhage- lipopolysaccharides (LPS) two hits rats. Methods Forty Wistar rats were divided randomly into 4 groups: sham operational group (S group) ; two hits groups with hemorrhage- LPS (HL group) ; dexamethasone preventive therapy group (HLD group) ; panaxadiol saponins preventive therapy group (HLP group). The rats were made first-hit by hemorrhagic shock, LPS were administered intraperitoneally to make endotoxic shock and induce two hits in rats, then the model of acute lung injury (ALI) induced by two hits had been built up successfully. NO2&-/NO3^- , MDA content and NOS, iNOS, SOD activities were measured by 722S spectrophotometer. Results The results of pathological observation showed that there was obvious inflammatory reaction in lung tissues after two-hits, and the structure was destroied. Compared with HL group, the inflammatory reaction was reduced in HLD group and HLD group. NOS, iNOS activities and NO2^-/NO3^- , MDA contents were increased significantly, and SOD activity was significantly lower in HL group compared with S group (P〈0.01); SOD activities in HLP group and HLD group were significantly higher than that in HL group (P〈0.01), and NOS, iNOS activities and NO2^-/NO3^-, MDA contents in HLP group and HLD group were significantly lower than those in HL group (P〈 0. 01). Conclusion Hemorrhage-LPS two hits could elevate significantly oxygen free radical in lung tissue, and cause lung injury, and PDS has protective effect on lung through anti-oxidative damage.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2008年第4期594-597,共4页
Journal of Jilin University:Medicine Edition
基金
吉林省科技厅自然科学基金资助课题(20030551-3)