红景天苷对缺氧/缺糖损伤神经细胞的保护作用

目的 :以SH-SY5Y细胞缺氧 /缺糖损伤为模型 ,观察红景天苷对神经细胞保护的作用。方法 :流式细胞术检测细胞凋亡百分率及细胞内 [Ca²⁺ ]i浓度 ,荧光显微镜观察细胞形态学变化和坏死百分率 ,用试剂盒显色法测定LDH的含量。结果 :缺氧 /缺糖损伤 2h可诱导神经细胞凋亡和坏死 ,分别为 18.5 9% (P<0.01)和 4 .94 % (P<0.01)。形态学观察也发现大量神经细胞染色质凝聚 ,核碎裂 ,凋亡小体产生 ,并显著增加细胞内 [Ca²⁺ ]i浓度和LDH的释放 ,分别为 8.46nmol·L^-1(PP<0.01)和 16 .5 9% (P<0.01) ,并随缺氧 /缺糖损伤时间的延长而明显增高 ;红景天苷 (1～ 3μmol·L^-1)能显著降低神经细胞凋亡及坏死的百分率 ,降低细胞内 [Ca²⁺ ]i浓度 ,减少LDH的释放 ,其作用随剂量增加而作用增强。结论 :红景天苷具有抑制SH-SY5Y细胞凋亡的作用 ,可对神经细胞起到保护作用 ,这种作用可能与其降低细胞内 [Ca²⁺ ]i浓度有关。

Protective effects of salidroside on injury induced by hypoxia/hypoglycemia in cultured neurons

Objective: To study the protective effects of salidroside on injury induced by hypoxia /hypoglycemia in cultured SH-SY5Y cell. Method: Apoptosis and intracellular free calcium concentration([Ca²⁺ ]i) were measured by flow cytometry, morphological changes and neuronal necrosis were observed with fluorescence microscope, and the lactic dehydrogenate (LDH) release was measured by LDH kits. Result: Hypoxia /hypoglycemia cultures for 2 hours induced neuronal apoptosis and necrosis. They were 18.59%( P <0.01) and 4.94%( P <0.01) respectively. There were morphological changes including chromatin condensation, nuclear fragmentation and formed apoptotic bodies after exposed to hypoxia /hypoglycemia for 2,4,6,12 hours. After 2 hours of hypoxia /hypoglycemia, neuronal [Ca ²⁺ ]i and the release of LDH were significantly increased .They were 8.46 nmol/L ( P<0.01) and 16.59%( P<0.01) respectively. The effects were enhanced with the extending time of hypoxia/hypoglycemia. Salidroside might have significantly decreased the percentage of neuronal apoptosis and necrosis, reduced neuronal [Ca ²⁺ ]i and the release of LDH. The effects of salidroside were strengthened with the increasing of Salidroside dosage. Conclusion: Salidroside has effect of anti-neuronal apoptosis. This effect might be related to its function of decreasing intracellular free calcium concentration.