摘要
目的探讨银杏内酯A(GKA)对凋亡海马神经细胞的影响及机制。方法用MTT法分析GKA对原代培养海马神经细胞的毒性作用,用浓度分别为0.1、1、10μmol/L的GKA预处理神经细胞6h,再用50μmol/LSNP孵育神经细胞24h;用流式细胞仪分析各组凋亡情况,用RT-PCR和Westernblot分析bcl-2、bax和cpp32 mRNA和蛋白表达水平,用试剂盒测定各组Cpp32活性。结果流式细胞术结果显示GKA实验组凋亡率均显著低于SNP组(P<0.01);RT-PCR结果和WesternBlot结果表明,GKA可以对抗SNP,上调bcl-2表达,下调bax表达,不影响Cpp32表达,但能显著降低Cpp32的活性(P<0.01)。结论GKA可以对抗SNP,对海马神经细胞有保护作用。
Objective Study the effects and mechanism of GKA against apoptosis of hippocampal neurons. Methods Neuronal viabihty was tested by MTT assay. After pre-treated with 0. 1,1,10 μmol/L GKA for 6 h, neurons were incubated with 50 μmol/L SNP for 24 h. The apoptosis of neurons were analyzed with flow cytometry;the expression levels of bcl-2 ,bax and cpp32 in mRNA and protein were analyzed with RT-PCR and Western blot. The activity of Cpp32 was determined by Kits. Results The apoptosis rates of GKA treated groups were lower than that of SNP group significantly（P 〈0.01 ） ;RT-PCR and Western blots indicated that GKA could counteract SNP and up-regulate the expressions of bcl-2 ,down-regulated the expressions of bax and not affect the expressions of cpp32 ;but GKA. could reduce the activity of Cpp32 significantly（ P 〈 0. 01 ）. Conclusions GKA can counteract the effects of SNP and protect hippocampal neurons against apoptosis.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2007年第16期1539-1541,共3页
Chinese Journal of Gerontology
基金
广东省重点学科资助(粤教科〔2004〕1号)
