摘要
目的观察刺五加多糖(ASPS)对H2O2诱导海马神经元氧化应激损伤及细胞凋亡相关基因-2(Bcl-2)家族的影响,并探讨其可能机制。方法运用海马神经细胞原代培养技术,采用H2O2诱导建立细胞氧化损伤模型。观察细胞形态学变化;MTT法测定细胞活性;TUNEL法,检测H2O2诱导大鼠海马神经元凋亡;免疫组化法检测细胞中Bc l-2,Bax蛋白表达;化学比色法检测细胞匀浆液中一氧化氮合酶(NOS),过氧化物歧化酶(SOD)的活性及丙二醛(MDA)含量。结果形态学观察显示:与模型组比较,ASPS组细胞损伤程度明显减轻;ASPS组细胞活性比模型组细胞活性高;TUNEL法显示ASPS预处理组细胞阳性率明显高于模型组细胞;ASPS组Bcl-2表达量较高而Bax表达量较低;NOS活力及MDA生成量ASPS组明显低于模型组,但SOD活力ASPS组显著高于模型组。结论ASPS能提高海马神经细胞的抗氧化应激损伤能力并上调Bcl-2基因表达,下调Bax表达。
Objective To observe the effects of Acanthopanacis senticosi polysaccharides on oxidative stress damage and Bcl - 2 family in hippocampal neurons impaired by H2O2 and to reveal the possible mechanism of this effect. Methods The model of oxidative damage was induced by H2O2. The change of cell morphology was observed ; the viability of hippocampal neurons was detected with MTT method ; apoptosis in hippocampal neurons induced by H2O2 was detected with TUNEL method, the expression of Bcl - 2 and Bax were detected by immunohistochemical method. The activity of NOS, SOD and the content of MDA in cell homogenate were determined by chemical chromatometry. Results Compared with model group, the morphology damage of hippocampal neurens was slighter than that in model group; the viability of hippocampal neurons in ASP groups（46% ） was higher than thatin model group（ 36% ） （P 〈 0.01 ） ;the rate of masculine in ASPS groups was obviously higher than that in model group with TUNEL method; ASPS could increase the expresion of Bcl -2 and decrease the expression of Bax. The activity of SOD in ASPS groupswas higher than that in model group , but the activity of NOS and the content of MDA in ASPS groups were significantly lower than those in model group. Conclusion ASPS can increase the capability of anti - oxidative stress damage in hippocampal neurons by up - regulating the expression of Bcl - 2 gene, and down - regulating the expression of Bax gene .
出处
《时珍国医国药》
CAS
CSCD
北大核心
2008年第11期2705-2707,共3页
Lishizhen Medicine and Materia Medica Research
基金
湖北省科技攻关计划(No.2006AA412C08)
