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目的观察脑神康胶囊对缺氧复氧损伤大鼠海马神经元凋亡及其Bcl-2、Bax mRNA表达的影响。方法随机将原代培养大鼠海马神经元分为对照组、损伤组、中药低、中、高浓度组。对照组正常培养,损伤组及中药组建立缺氧复氧损伤模型,中药各浓度组于复氧时换以不同浓度含药血清的培养液,采用MTT法测各组细胞存活率,采用流式细胞仪检测凋亡率,采用RT-PCR法检测Bcl-2和Bax mRNA的表达并计算两者比值。结果损伤组细胞存活率及Bcl-2 mRNA表达明显下降(P均<0.01),凋亡率及Bax mRNA表达显著升高(P均<0.01),Bcl-2/Bax降低(P<0.01);中药各浓度组较损伤组细胞存活率及Bcl-2 mRNA表达均升高(P均<0.01),凋亡率及Bax mRNA表达降低(P<0.01,P<0.05),Bcl-2/Bax增加(P<0.01),且呈明显的剂量依赖性。结论脑神康胶囊对海马神经元缺氧复氧损伤有明显的保护作用,其作用机制可能与其调节凋亡相关蛋白、减少凋亡密切相关。
Objective To observe the effect of Naoshenkang capsule on the apoptosis of hippocampal neurons and the expression of Bcl-2 and Bax mRNA in rats with hypoxia-reoxygenation injury. Methods The primary cultured rat hippocampal neurons were randomly divided into control group, injury group, low, middle and high concentrations of traditional Chinese medicine. The normal culture, the injury group and the Chinese medicine group in the control group were established the hypoxia-reoxygenation injury model. The concentration of each concentration group of the Chinese medicine was changed to the culture medium with different concentrations of drug-containing serum at the time of reoxygenation. The cell survival rate was measured by the MTT method and the flow rate was adopted. Cytometry was used to detect the apoptosis rate. The expression of Bcl-2 and Bax mRNA was detected by RT-PCR and the ratio between them was calculated. Results The cell viability and the expression of Bcl-2 mRNA in the injury group were significantly decreased (P<0.01), the apoptosis rate and Bax mRNA expression were significantly increased (P<0.01), Bcl-2/Bax was decreased (P<0.01). The cell survival rate and the expression of Bcl-2 mRNA were higher in each concentration group than in the injury group (P<0.01), the apoptosis rate and Bax mRNA expression were decreased (P<0.01, P<0.05), and the Bcl-2/Bax increased. (P<0.01), and showed significant dose dependence. Conclusion Naosgang Capsule has obvious protective effect on hippocampal neurons against hypoxia/reoxygenation injury. The mechanism may be related to its regulation of apoptosis-related proteins and decreased apoptosis.