人参总皂苷对大鼠创伤性脑水肿的影响

目的研究人参总皂苷对创伤性脑损伤(TBI)大鼠脑组织中水含量、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的含量及神经功能的影响,以探讨人参总皂苷治疗大鼠创伤性脑水肿的作用及可能的机制。方法采用改良Feeney DM法建立大鼠TBI模型,将动物随机分为假手术组、脑外伤组、人参总皂苷治疗组。所有动物分别于伤后1、3、5、7d进行神经行为学评分后处死,取损伤区脑组织,采用干湿重法测脑水含量,生物化学法测脑组织中SOD活性和MDA含量,ELISA法测定脑组织中TNF-α、IL-1β的表达水平。结果与脑外伤组同期比较,人参总皂苷治疗组脑水含量和MDA含量降低,SOD活性升高,脑组织内TNF-α、IL-1β的水平明显降低(P<0.05),神经功能改善明显(P<0.05)。结论人参总皂苷能明显减轻创伤性脑损伤后脑水肿的程度,减轻神经行为缺损症状,其机制可能是通过减少脑组织中MDA生成,降低IL-1β、TNF-α的表达,提高SOD活性,抑制自由基反应,减轻炎症反应而起作用。

Effects of Ginseng Total Saponin on Traumatic Brain Edema of Rats

Objective To observe the effects of ginseng total saponin （GTS） on the water content in the brain tissue, the activity of superoxide dismutase （SOD）, the content of malondialdehyde （MDA）, the expression levels of tumor necrosis factor a （TNF-α） and interleukin 1β （IL-1β）, and the neurological function in rats with traumatic brain injury （TBI）, and to explore the roles of GTS in treating traumatic brain edema rats and its possible mechanisms. Methods The TBI rat model was established using modified Feeney＇s method. Rats were randomly divided into 3 groups, i.e., the sham-operation group, the TBI group, and the GTS-treated group. All rats were sacrificed after their neurological behavior was scored at day 1, 3, 5, and 7 of TBI. The brain tissue was taken out to measure the brain water content with wet-dry weight method. The activity of SOD in the brain tissue and the content of MDA were determined using biochemistry method. The expression levels of TNF-α and IL- 1β in the brain tissue were detected using ELISA. Results Compared with the TBI group at the same time point, the brain water content and the content of MDA decreased, the activity of SOD increased, the expression levels of TNF-α and IL-1β obviously decreased, and the neurological functions were obviously improved in the GTS- treated group （ P 〈0.05）. Conclusions GTS could obviously alleviate the degree of traumatic brain edema after TBI, and attenuate the deleted neurological behavioral symptoms. The underlying mechanisms might be achieved through reducing the production of MDA, decreasing the expression levels of TNF-α and IL-1β, elevating the activity of SOD, inhibiting free radical reaction, and alleviating inflammatory reactions.