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目的 观察丹参素对SH SY5Y细胞缺氧 缺糖损伤时胞浆内 [Ca2 + ]i、细胞凋亡率、细胞活性和线粒体膜电位的变化 ,探讨其对神经细胞线粒体的保护作用及其可能的机理。方法 应用细胞培养、四唑盐比色实验 (MTT)检测细胞活力 ,流式细胞术检测细胞内 [Ca2 + ]i、细胞凋亡百分率和线粒体膜电位。结果 SH SY5Y细胞缺氧 缺糖损伤 2h时 ,细胞内 [Ca2 + ]i明显增加 ,为 8 4 6nmol L(P <0 0 1) ,细胞凋亡率明显增高 ,为 18 5 9% (P <0 0 1) ,细胞内 [Ca2 + ]i的浓度 4h时达到高峰 ,为 9 89nmol L(P <0 0 1) ,而后呈下降趋势 ,细胞凋亡率随缺氧 缺糖损伤时间的延长而明显增高12h时达到 4 5 91% ,细胞经缺氧 缺糖处理 2h后 ,线粒体膜电位和细胞活性分别降低 2 9 17% (P<0 0 1)、38 80 % (P <0 0 1) ,随着缺氧 缺糖时间的延长线粒体膜电位和细胞活性进一步下降 ,12h时分别降低 5 6 72 % (P <0 0 1)、6 3 5 8% (P <0 0 1) ,丹参素能显著降低细胞内 [Ca2 + ]i,抑制细胞凋亡的发生 ,提高细胞活性和线粒体膜电位 ,与缺氧 缺糖组相比均有显著性差异 (P <0 0 5 ,P <0 0 1)。结论 丹参素可抑制缺氧 缺糖损伤所致的线粒体膜电位的降低 ,从而具有稳定线粒体膜电位的作用 ,抑制细胞凋亡的发生 ,这种作用可
Objective To observe the change of cytosolic [Ca2 + ]i, apoptosis rate, cell viability and mitochondrial membrane potential of SH SY5Y cells during hypoxia- glucose deprivation injury, and to explore its protective effect on neuronal mitochondria and its possible mechanism. mechanism. Methods The cell viability was detected by cell culture and tetrazolium salt colorimetric assay (MTT). The intracellular [Ca2 +]i, apoptosis and mitochondrial membrane potential were detected by flow cytometry. Results When SH SY5Y cells were injured by oxygen-glucose deprivation for 2 h, the intracellular [Ca2 +] i increased significantly, being 846 nmol L (P <0 01), and the cell apoptosis rate was significantly higher, which was 18 5 9% (P < 0 0 1) , the [Ca2 +]i concentration in the cell reached a peak at 9 h, which was 9 89 nmol L (P <0 01), and then decreased. The apoptotic rate was associated with the prolongation of hypoxia and glucose deprivation. The mitochondrial membrane potential and cell viability were decreased by 2 9 17% (P<0 01) and 38 80% (P <0 01), respectively. The mitochondrial membrane potential and cell activity further decreased with the increase of hypoxia/glucose deprivation time, and decreased by 656 2% (P <0 01), 6 3 5 8% (P <0.01) at 12 hours, and Danshensu Can significantly reduce intracellular [Ca2 +] i, inhibit the occurrence of apoptosis, increase cell viability and mitochondrial membrane potential, compared with the oxygen deficiency and glucose deprivation group were significantly different (P <0 0 5, P <0 0 1). Conclusion Danshensu can inhibit the decrease of mitochondrial membrane potential induced by hypoxia and glucose deprivation, which can stabilize the mitochondrial membrane potential and inhibit the occurrence of apoptosis.