摘要
目的:观察银杏内酯B(GKB)对体外分化的神经干细胞(NSC)神经突起生长的影响,并初步探讨其可能的机制。方法:用含不同浓度(20 mg/L、40 mg/L、60 mg/L)GKB的分化培养基培养NSC,在不同时间点测量细胞突起的数量和长度,在第7天时应用免疫荧光染色法检测细胞因子信号转导抑制因子-2(SOCS2)表达。结果:(1)24 h和3 d时各GKB组NSC神经突起长度和数量均较对照组显著增加(P<0.01);40 mg/L和60 mg/L GKB组NSC神经突起数量和平均长度较20 mg/L GKB组显著增加(P<0.01),但两者之间无显著差异。(2)各GKB组和对照组3 d时NSC神经突起长度比24 h时显著增加(P<0.01);对照组3 d时NSC神经突起数量与24 h时无显著差异,而相同GKB组间NSC平均神经突起数量均显著增加(P<0.01)。(3)各GKB组SOCS2免疫反应物平均吸光度分别为1.382、1.578和1.527,均显著高于对照组(1.134,P<0.01);40 mg/L和60 mg/L GKB组SOCS2免疫反应物平均吸光度显著高于20 mg/L GKB组(P<0.01),但40 mg/L GKB组与60 mg/L GKB组无显著差异。结论:GKB能够促进体外分化的NSC神经突起生长,表现为神经突起数量和长度增加;其作用机制可能与SOCS2表达上调有关。
Objective： To observe the effect of Ginkgolide B （GKB） on neurite outgrouth of neural stem cells （NSCs） differentiated in vitro and to preliminarily explore its possible mechanism. Methods： NSCs were cultured by using GKB differentiation medium containing different concentrations （20 mg/L, 40 mg/L, and 60 mg/L）. The numbers and lengths of neurite were measured at different time points. Immunofluorescent staining was used to detect the expression of suppressors of cytokine signaling-2 （SOCS2） on day 7. Results： （1） the numbers and lengths of neurite in all the GKB groups at 24 hours and day 3 were significantly more and longer than those in the control group （P 〈0.01 ）; the numbers and average length of neurite in the 40 mg/L and 60 mg/L GKB groups were significantly more and longer than those in the 20 mg/L GKB group （P 〈 0.01 ）, but there were no significant differences between them. （2） The lengths of neurite at day 3 in all the GKB and control groups were significantly longer than those at 24 hours （P 〈0.01）; there were no significant differences between the numbers of neurite at day 3 and at 24 hours in the control group （P 〉 0.05）, while the NCS average number of neurite between the same GKB groups was significantly increased （P 〈 0.01 ）. （3） The average absorbency of SOCS2 immunoreactive products in all the GKB groups were 1. 382, 1. 578, and 1. 527 respectively, and they were all significantly higher than that in the control group （1.134, P 〈 0.01 ）; the average absorbency of SOCS2 immunoreactive products in 40 mg/L and 60 mg/L GKB groups was significantly higher than that in the 20 mg/L GKB group （P 〈 0. 01 ）, however, there were no significant differences between 40 mg/L and 60 mg GKB groups. Conclusions： GKB promotes neurite outgrowth of NSCs differentiated in vitro by increasing the numbers and lengths of neurite. Its mechanism of action may be associated with the upregulation of SOCS2 expression.
出处
《国际脑血管病杂志》
2007年第10期739-743,共5页
International Journal of Cerebrovascular Diseases
基金
国家自然科学基金资助(30371630
30672732)
