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机构地区:[1]咸宁学院医学院组织学与胚胎学教研室,咸宁437100
出 处:《解剖学杂志》2005年第3期332-334,i002,共4页Chinese Journal of Anatomy
基 金:湖北省自然科学基金(98A078)
摘 要:目的:观察烫伤大鼠小肠肌间神经丛Bax/Bcl-2蛋白的表达特征,了解银杏叶提取物(EGb)干预的作用机制。方法:动物分烫伤组和治疗组,各组于不同时间点处死、取材,制成肠肌间神经丛铺片。采用免疫组织化学方法,进行Bax/Bcl-2检测。结果:Bax/Bcl-2的表达是以烫伤后24h阳性最强,以后随着时间延长而逐渐下降;治疗组较对应时间点的烫伤组Bax阳性信号明显减弱,Bcl-2阳性信号明显增强。结果:细胞凋亡是大鼠严重烫伤后小肠肌间神经丛神经元丢失的重要原因,而Bax/Bcl-2是参与神经细胞凋亡的重要凋亡调控基因。并推测EGb具有显著的保护作用,其机制可能与影响Bax/Bcl2基因表达,而起到保护烫伤后迟发性神经细胞死亡的作用有关。Objective: To observe Bax/Bcl-2 protein expression in the intestinal myenteric plexus in burned rats and the protective effect of Ginko biloba extract (Egb 761). Methods: Healthy SD rats were randomly divided into control group, burned group and treated group. Each group was further divided into 24, 48 and 72 h post-burn subgroups. The rats were anaesthetized and fixed. Intestine was taken out, and then the intestine was fixed for 4 h (4℃) again.The outer longitudinal tunica muscularis was peeled carefully from the ring tunica muscularis and submucosa. Immunohistochemistry staining was used to detect Bax/Bcl-2 protein expression in the intestinal myenteric plexus. Results: A significant increase of Bax/Bcl-2 expression was detected at 24 h post-burn, and it began to decrease at 48 h post-burn and decreased to a much lower level at 72 h post-burn. Compare with those in the burned group, expression of Bax and the Bcl-2 in treated group was weakened and obviously strengthened respectively. Conclusion: Apoptosis is the main cause of neuronal loss in the intestinal myenteric plexus in burned rats. The Bax/Bcl-2 is an important regulation gene participating in the apoptosis. It is deduced that the EGb has protective effects against apoptosis, whose protective mechanism might be related to improved blood circulatory and increased volume of intestinal blood flow.
关 键 词:小肠肌间神经丛 银杏叶提取物 保护作用 烫伤大鼠 bcl-2表达 Bax/Bcl-2蛋白 bax BCL-2基因表达 迟发性神经细胞死亡 免疫组织化学方法 凋亡调控基因 神经细胞凋亡 阳性信号 神经元丢失 表达特征 作用机制 不同时间 时间延长
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