神经细胞缺氧/缺糖损伤后阿司匹林的线粒体保护研究

Neuroprotective effect of aspirin on neuronal mitochondria following oxygen/glucose deprivation-induced injury

目的观察神经细胞缺氧/缺糖损伤后线粒体膜电位(MMP)和凋亡的变化情况及阿司匹林的保护作用。方法用体外培养7 d的Wistar大鼠皮质神经细胞,随机分为正常对照组、缺氧/缺糖模型组、缺氧/缺糖加100μmol/L浓度阿司匹林组。缺氧/缺糖2 h处理后,四甲基偶氮唑盐(MTT)比色分析法检测神经元线粒体活性;流式细胞术检测神经元线粒体膜电位、双染法检测不同组神经元的凋亡情况。结果缺氧/缺糖损伤2 h后,模型组的线粒体活性和MMP水平较对照组显著降低(P<0.01)。细胞凋亡百分率均较对照组显著升高(P<0.01)。而阿司匹林组能显著提高神经元线粒体活性、膜电位,降低细胞凋亡的百分率。结论阿司匹林可抑制缺氧/缺糖损伤所致的神经元线粒体活性和膜电位的降低、稳定线粒体膜电位,抑制神经元凋亡,起到神经元保护作用。

Objective To investigate the neuroprotective effects of aspirin on mitochondrial membrane potential （MMP） and apoptosis following oxygen/glucose deprivation （OGD）-induced injury in neurons. Methods Cultured cor-tex neurons harvested from Wistar rats at day 7 were randomly assigned to normal control group, OGD group, and OGD plus aspirin treatment （100 μmol/L） group, respectively. Following OGD for 2 hours, mitochondrion activity was measured based on the methyl thiazolyl tetrazolium （MTT） test. The MMP was measured by flow cytometry. Neuronal necrosis were assayed with annexin-FITC and PI double immunofluorescence microscopy. Results Following OGD for 2 hours, the MMP and mitochondrion activity were consistently reduced and the percentage of neuronal apoptosis increased （all P〈0.01）. Aspirin significantly restored mitochondrion activity, decreased the percentage of neuron apop-tosis, and increased the MMP. Conclusion Aspirin significantly abrogates the decline of MMP, restores mitochondri-on activity, stabilizes the MMP and inhibits neuronal apoptosis following OGD induced injury, which represents the neuroprotective effects.