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目的以缺氧、缺糖再给氧为模型,观察清开灵注射液对大鼠海马神经细胞凋亡和线粒体膜电位的影响。方法四唑盐比色实验(MTT)检测细胞线粒体活性,流式细胞术检测细胞凋亡百分率和线粒体膜电位,荧光显微镜观察细胞形态学变化和坏死百分率。结果缺氧、缺糖5 h再给氧3、12、24 h时,细胞凋亡率明显增高,形态学观察也发现大量神经细胞的染色质凝聚、核碎裂、凋亡小体产生;细胞线粒体膜电位和活性均显著降低,随再给氧时间的延长而进一步下降,清开灵注射液能显著降低神经细胞凋亡及坏死的百分率,提高线粒体膜电位和活性,与缺氧、缺糖再给氧组相比均有显著性差异(P<0.05~0.01)。结论清开灵注射液可抑制缺氧、缺糖再给氧损伤所致的线粒体膜电位降低,从而稳定线粒体膜电位、抑制细胞凋亡的发生,而对海马神经细胞起到保护作用。
Objective To observe the effects of Qingkailing injection on hippocampal neuronal apoptosis and mitochondrial membrane potential in a model of hypoxia, hypoglycemia and reoxygenation. Methods Cell mitochondrial activity was measured by tetrazolium salt colorimetric assay (MTT). Apoptosis percentage and mitochondrial membrane potential were detected by flow cytometry. Morphological changes and percentage of necrosis were observed by fluorescence microscope. RESULTS: Apoptosis rate increased significantly after hypoxia and glucose deprivation for 3 h, 3 h, 12 h, and 24 h, and morphological observations also revealed a large number of neurons with chromatin condensation, nuclear fragmentation, and apoptotic bodies; The mitochondrial membrane potential and activity both decreased significantly and decreased further with prolonged reoxygenation time. Qingkailing injection can significantly reduce the percentage of apoptosis and necrosis of nerve cells, increase mitochondrial membrane potential and activity, and lack of oxygen and sugar. Compared with the oxygen group, there was a significant difference (P<0.05~0.01). Conclusion Qingkailing injection can inhibit the decrease of mitochondrial membrane potential induced by hypoxia, glucose deprivation and reoxygenation injury, stabilize the mitochondrial membrane potential, inhibit the occurrence of apoptosis, and protect the hippocampal neuronal cells.