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目的研究低分子量姬松茸多糖(LMPAB)对氧应激大鼠海马神经元Bcl-2和Bax表达的影响。方法取24 h内出生大鼠的海马神经元细胞原代培养,分为对照组、模型组、3个剂量实验组(LMPAB,3,5,10,20 mg·L~(-1))。实验组预处理24 h后,同模型组均加入500μmol·L~(-1) H_2O_2损伤2 h。用流式细胞术和MTT法检测大鼠海马神经元细胞凋亡及细胞活性,用免疫细胞化学检测Bcl-2和Bax蛋白的表达。结果海马神经元凋亡率,高剂量组(10.08±0.83)显著低于模型组(29.01±0.67,P<0.01);细胞活力,高剂量组(0.38±0.05)显著高于模型组(0.20±0.07,P<0.01);与模型组相比,高剂量组Bcl-2表达显著增高(42.73±3.65 vs 29.43±2.26),Bax表达显著降低(22.47±2.82 vs47.58±4.79)(均P<0.01),Bcl-2/Bax比率增高。结论 LMPAB对氧化应激损伤的大鼠海马神经元有一定的保护作用,其机制可能与抑制海马神经元凋亡有关。
Objective To investigate the effect of low molecular weight Agaricus blazei polysaccharide (LMPAB) on the expression of Bcl-2 and Bax in hippocampal neurons of oxygen-stressed rats. Methods Primary cultured hippocampal neurons of rats born within 24 h were divided into control group, model group and three dose groups (LMPAB, 3,5,10,20 mg · L -1). After pretreatment for 24 h in experimental group, 500 μmol·L -1 H 2 O 2 injury was induced in the same model group for 2 h. The apoptosis and cell viability of hippocampus neurons were detected by flow cytometry and MTT assay. The expressions of Bcl-2 and Bax protein were detected by immunocytochemistry. Results The apoptotic rate of hippocampal neurons in high dose group (10.08 ± 0.83) was significantly lower than that in model group (29.01 ± 0.67, P <0.01). The cell viability and high dose group (0.38 ± 0.05) 0.07, P <0.01). Compared with the model group, the expression of Bcl-2 in high-dose group was significantly higher (42.73 ± 3.65 vs 29.43 ± 2.26) and significantly lower in Bax (22.47 ± 2.82 vs 47.58 ± 4.79, P < 0.01), Bcl-2 / Bax ratio increased. Conclusion LMPAB may protect hippocampal neurons from oxidative stress injury in rats, which may be related to the inhibition of apoptosis in hippocampal neurons.