山药多糖抗神经细胞缺氧性凋亡机制研究  

Effect of polysaccharide from Yam against neuron apoptotic induced by hypoxia

作　　者：向勤[1] 蒲明[2] 胡微煦[3] 文珠 何丹[2] 胡国柱[2] 

机构地区：[1]南昌大学研究生院医学部,江西南昌330006 [2]江西省人民医院,江西南昌330006 [3]复旦大学上海市肿瘤医院,上海200032 [4]江西省医学科学研究院,江西南昌330006

出　　处：《中成药》2013年第12期2564-2569,共6页Chinese Traditional Patent Medicine

基　　金：江西省科技厅社会发展计划(2007BS22602)

摘　　要：目的探讨山药多糖抗神经细胞缺氧性凋亡作用机制。方法运用SD胎鼠大脑皮层神经细胞建立缺氧性神经细胞损伤体外模型,再使用不同质量浓度山药多糖处理,Rh-123染色检测线粒体损伤,RT-PCR及免疫细胞化学测定Caspase-3、Bax、Bcl-2 mRNA及蛋白表达。结果山药多糖抑制缺氧的神经细胞线粒体损伤,下调Caspase-3蛋白及mRNA的表达,下调Bax mRNA及蛋白的表达,上调Bcl-2 mRNA及蛋白的表达,提高Bcl-2/Bax mRNA及蛋白的比例(P<0.05)。结论山药多糖在一定发范围内能有效地抑制神经细胞缺氧性凋亡,其机理是降低凋亡基因及蛋白产生,上调抗凋亡基因及蛋白产生。AIM To explore the protective effect of polysaccharide from Yam on the neuron apoptosis induedby hypoxia. METHODS Neural cells in cortical neurous isolated from SD rat embryos were applied to establis- hing the model for the hypoxic nerve cell damage, and then obtained nerve cells were treated with polysaccharide from Yam of various concentrations. Mitochondria injury was examined by Rhodamine 123 staining in flow cytome- try. The mRNA and protein expressions of Caspase-3, Bax, Bcl-2 were identified by RT-PCR and immunocyto- chemistry. RESULTS The mitochondria injury was significantly inhibited , the levels of caspase-3 and Bax mR- NAs and proteins were significantly down-regulated by polysaccharide from Yam, the levels of Bcl-2 mRNA and protein were significantly up-regulated, and the ratio of Bcl-2/Bax in mRNA and protein were significantly elevated by polysaccharide from Yam （P 〈 0. 05）. CONCLUSION Polysaccharide from Yam has an inhibitory effect on apoptosis of neurons caused by hypoxia, due to the decrease in levels of apoptotic genes and proteins and the in- crease in levels of anti-apoptotic gene and protein in hypoxic neurons.

关 键 词：山药多糖 神经细胞 缺氧 凋亡 线粒体 半胱氨酸天冬氨酸蛋白酶一3(Caspase一3) B淋巴细胞瘤-2基因相关蛋白(BCL-2一associatedXprotein Bax) B淋巴细胞瘤_2基因(Bcl-2) 体外 

分 类 号：R285.5[医药卫生—中药学]