三七皂甙对脑水肿大鼠保护作用的机制

背景脑水肿使颅内压明显增高和神志障碍,严重可导致脑疝,这些病理变化是造成脑功能障碍的主要原因.应用三七皂甙治疗脑水肿是目前国内外研究热点,具有重大理论意义.目的探讨三七皂甙对百日咳菌液致大鼠脑水肿的治疗作用及机制.设计随机对照研究.地点和对象实验地点中南大学湘雅医学院机能实验室.健康SD大鼠40只,随机分为生理盐水组、百日咳菌液组、三七皂甙组、甘露醇组4组.干预采用百日咳菌液注入左颈内动脉导致大鼠脑水肿.主要结局观察指标各组大鼠左脑组织含水量、伊文思蓝、丙二醛水平、超氧化物歧化酶(superoxidedismutase,SOD)活性、肿瘤坏死因子α(tumor necrosisfactor-α,TNFα)水平.结果左脑组织TNFα水平,三七皂甙组(457.9±92.6)Pg/g明显低于百日咳菌液组(725.6±76.3)pg/g和甘露醇组(686.4±102.1)Pg/g(q=3.52～4.18,P＜0.05).左脑组织的含水量生理盐水组(78.8±0.3)%、三七皂甙组(79.8±0.4)%和甘露醇组(82.2±0.3)%均较百日咳菌液组(83.9±0.2)%为低(q=3.64～4.56,P＜0.05),三七皂甙组较甘露醇组低(q=3.38,P＜0.05).左脑组织的伊文思蓝含量生理盐水组(1.9±0.7)μg/g、三七皂甙组(5.2±0.9)μg/g和甘露醇组(8.4±0.6)μg/g均较百日咳菌液组(12.1±0.5)μg/g低(q=3.82～4.45,P＜0.05),三七皂甙组较甘露醇组为低(q=3.66,P＜0.05).治疗各组均能降低丙二醛水平,提高SOD活性(q=3.42～4.19,P＜0.05).结论三七皂甙对百日咳菌液致大鼠脑水肿具有治疗作用,其机制与抑制脂质过氧化和减少TNFα生成有关.

Protective mechanism of panax notoginseng saponin against brain edema in rats

BACKGROUNDS: The brain edema results in remarkable increasing of intracranial pressure, mental disturbance and even cerebral hernia in the severe case. Those pathological changes are known as the essential factors for the cerebral functional disturbance. Researches on the treatment of panax notoginseng saponin for brain edema is the hotspot at present at home and abroad with great significance theoretically.OBJECTIVE: To explore the treating action and mechanism of panax notoginseng saponin(PNGS) on rat brain edema induced by pertussis bacterial(PB)liquid.DESIGN: Randomized controlled study.SETTING and MATERIALS: The experiment was performed in the Function Laboratory in Xiangya Medical College of Central South University. 40normal SD rats were randomized into 4 groups, namely normal saline(NS)group, PB group, PNGS group and mannitol(MN) group.INTERVENTION: PB was injected into the left internal carotid artery of the rat inorder to induce brain edema.MAIN OUTCOME MEASURES: The contents of water and Evans blue,the level of malondieldehyde(MDA), superoxide dismutase(SOD) activity,and the level of tumor necrosis factor-α(TNFα) in the left brain tissue in each group.RESULTS: TNFo level in the left brain tissue in the PNGS group[ (457.9 ±92.6) pg/g] was remarkably lower than that in the PB group[(725.6 ±76.3) pg/g] and the MN group[ (686. 4 ±102.1) pg/g] (q=3.52-4. 18, P ＜ 0.05) respectively. The water contents in the NS group[ (78. 8 ±0.3)%, PNGS group[(79.8±0.4)% ] and MN group[(82.2±0.3)% ]were lower than that in PB group[ (83.9 ± 0. 2) % ] ( q = 3.64 - 4. 56, P ＜0.05) successively, and that in PNGS group was lower than that in MN group ( q = 3.38, P ＜ 0.05) . The contents of Evans blue in the NS group[ (1.9 ±0.7) μg/g], PNGS group[(5.2±0.9) μg/g] and MN group[(8.4±0. 6) μg/g] were lower than that in PB group[ (12. 1 ± 0. 5 )μg/g] ( q = 3. 82 -4.45, P ＜ 0. 05) successively, which were lower in PNGS group as compared with MN group( q = 3.66, P ＜ 0.05). The treatment reduced the level of MDA and increased SOD activity in each group( q = 3.42 - 4. 19, P ＜ 0.05).CONCLUSION: PNGS plays a role in the treatment of rat brain edema induced by PB, whose mechanism is related to lipid eroxydation inhibition and alleviating TNFα formation.