黄芩苷对Neuro2A细胞氧糖剥夺的保护作用

Protective effects of baicalin on Neuro2A cells under oxygen and glucose deprivation

目的观察黄芩苷对体外培养小鼠神经母细胞瘤Neuro2A细胞株氧糖剥夺所致损伤的保护作用。方法利用体外培养的Neuro2A细胞,通过去除培养液中的糖和氧气来模拟脑缺血缺氧,用不同浓度的黄芩苷作用于Neuro2A细胞,应用Annexin V-FITC/PI染色,流式细胞术检测细胞凋亡,应用四唑盐(MTT)法检测细胞的活性。结果黄芩苷在6.25,12.5,25μmol.L-1的浓度范围之内,可对缺血缺氧Neuro2A细胞起到保护作用,主要是减少细胞早期凋亡。结论在一定浓度范围之内黄芩苷可保护缺血缺氧Neuro2A细胞,提示对缺血性脑损伤有保护作用,值得进一步研究。

Aim Neural injury in the central nervous system following is chemic insult is believed to result from oxygen and glucose deprivation. In this study, baicalin was investigated for its neuroprotective effects against oxygen and glucose deprivation （OGD） in Neuro2A cells. Methods Mitochondrial activity was assessed with 3- （ 4,5-dimethylthiazol-2-yl ） -2,5-diphenyl tetrazolium bromide （MTT） reduction activity assay. Apoptosis was monitored with flow cytometry. It was found that baicalin increased MTT reduction activity and decreased percentage of apoptosis of the cultured Neuro2A cells. Results Baicalin showed significant protective effects on the OGD-induced apoptosis in cultured Neuro2A cells. Conclusion These results suggest that baicalin is an effective compound in preventing neurotoxicity induced by OGD and therefore deserves further scrutiny.