摘要
目的探讨人参皂甙Rd(GSRd)对大鼠癫癎持续状态后齿状回netrin-1表达及海马神经元凋亡的影响。方法健康Wistar大鼠30只,随机分为颞叶癫癎组、GSRd组和对照组,每组10只。氯化锂-匹罗卡品建立大鼠颞叶癫癎模型,采用免疫组织化学法及TUNEL法观察颞叶癫癎组、GSRd组和对照组齿状回netrin-1蛋白表达及海马神经元凋亡细胞数情况。结果与对照组比较,颞叶癫癎组大鼠30 d齿状回netrin 1蛋白表达明显增高,海马CA3区TUNEL阳性细胞数在癫癎持续状态后7 d明显增高,差异有统计学意义(P<0.05);与颞叶癫癎组比较,GSRd组大鼠30 d齿状回nctrin l蛋白表达明显降低,海马CA3区TUNEL阳性细胞数在癫癎持续状态后7 d明显降低,差异有统计学意义(P<0.05)。结论 GSRd可能通过下调netrin 1的表达,并使神经元凋亡数目减少,从而发挥对神经元的保护作用。
Objective To investigate the effects of ginsenoside-Rd(GSRd) on the expression levels of netrin-1 and neuron apoptosis in the rat hippocampus after lithium-pilocarpine induced epilepsy. Methods Thirty Wistar rats were randomly divided into the NS control group,temporal lobe epilepsy(TLE) group and GSRd group. The TLE animal model was established using lithium-piloearpine. Netrin-I proteins were detected with immunohistochemieal method. The neuron apoptosis was observed with TdT-mediated dUTP nick end labeling(TUNEL) method. Results The ex- pression of netrin-1 in GSRd group was notably lower than that of TLE group (P 〈 0.05). The TUNEL positive cells in hippoeampus CA3 of TLE group were more than those of NS control group (P 〈 0.05). TUNEL positive cells in TLE group were significantly more than those in NS control group (P 〈 0.05). TUNEL positive cells in GSRd treated group significantly decreased as compared with TLE group (P 〈 0.05). Conclusions GSRd may serve as an effective agent for curing the brain damage after TLE in vivp . The mechanism of protecting the neuron may include downregulating the expression of netrin-1 and reducing the number of apoptotic neurons.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2011年第5期460-462,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词
人参皂甙类
癫痫
神经元
海马
细胞凋亡
氯化锂
模型
动物
ginsenosides
epilepsy
neurons
hippocampus
apoptosis
lithium chloride
models, animal