摘要
目的:观察黄芪总皂苷合三七总皂苷(TSA+PNS)对脑缺血再灌注致脂质过氧化反应的影响,初步探讨其机制。方法:结扎大鼠的双侧颈总动脉,复制脑缺血再灌注病理模型,静脉注射给药,观察再灌注后脑组织乳酸脱氢酶(LDH)活力、超氧化物歧化酶(SOD)活力、丙二醛(MDA)浓度的变化。采用Fe^2+-H2O2体系产生羟自由基、黄嘌呤-黄嘌呤氧化酶体系产生超氧阴离子、Fe^2+-H2O2诱导脑组织脂质过氧化,观察TSA+PNS对其的影响。结果:与假手术组比较,模型动物脑组织MDA明显升高(P〈0.01),LDH活力、SOD活力明显降低(P〈0.01);应用TSA+PNS后,可提高SOD、LDH活力,降低MDA含量。体外实验,TSA+PNS显著抑制脂质过氧化、羟自由基、超氧阴离子的产生(P〈0.05-0.01)。结论:TSA+PNS对脑缺血再灌注导致的脂质过氧化反应有抑制作用,清除超氧阴离子、羟自由基是其重要的作用机制。
Objective:To observe the influence of TSA and PNS on lipid peroxidatic reaction of experimental cerebral ischemia reperfusion, and approach the mechanism. Method: Rat' s bilateral arteria carotis communis were deligated to reproduce pathology model of cerebral ischemia reperfusion. Administer by intravenous injection. And observe LDH, SOD and MDA in brain tissue after reperfusion. By Fe^2+ -H2O2 system generating hydroxy radical, xanthinexanthine oxidase system generating superoxide anion, and Fe^2+ -H2O2 inducing brain tissue lipid peroxidation, observe the influence of TSA and PNS on them. Result: Comparing with sham operated group, MDA in model rat's brain tissue was improved remarkably (P 〈0. 01 ). Motoricity of LDH and SOD was degraded remarkably (P 〈0. 01 ). After TSA and PNS were administered, motoricity of LDH and SOD was improved and content of MDA was degraded. In extraorgan experiment, TSA and PNS inhibited notably to generate lipid peroxidation, hydroxy radical and superoxide anion (P 〈 0. 05-0. 01 ). Conclusion: TSA and PNS can inhibit the reaction of lipid peroxidation resulted from cerebral ischemia reperfusion, and the important mechanism is to remove superoxide anion and hydroxy radical.
出处
《山西中医》
2008年第5期48-50,共3页
Shanxi Journal of Traditional Chinese Medicine
关键词
三七总皂苷
黄芪总皂苷
脑缺血再灌注
脂质过氧化
超氧阴离子
羟自由基
实验研究
astragali total saponin and notoginseng total saponin (TSA and PNS), cerebral ischemia reperfusion, lipid peroxidation, superoxide anion, hydroxy radical