摘要
目的 :观察红景天甙对SH -SY5Y细胞缺氧 /缺糖损伤时细胞内 [Ca2 + ]i、细胞凋亡率、细胞线粒体膜电位和活性的变化 ,探讨其对神经细胞线粒体膜电位的影响。方法 :应用细胞培养 ,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 2、4、6、12h后 ,细胞内 [Ca2 + ]i和细胞凋亡百分率明显高于对照组 ,均有显著差异 (P <0 0 1) ;细胞经缺氧 /缺糖处理后 ,线粒体膜电位和活性明显低于对照组 ,2h时分别为 2 9 17% (P <0 0 1) ,38 80 % (P <0 0 1) ,12h时分别为5 6 72 % (P <0 0 1) ,6 3 5 8% (P <0 0 1) ;红景天甙能显著降低细胞内 [Ca2 + ]i,抑制细胞凋亡的发生 ,提高线粒体膜电位和活性 ,与缺氧 /缺糖损伤组相比均有显著差异 (P <0 0 5 ,P <0 0 1)。结论 :红景天甙可抑制缺氧 /缺糖损伤所致的线粒体膜电位和活性的降低 ,从而具有稳定线粒体膜电位的作用 ,抑制细胞凋亡的发生 。
AIM: To investigate the effects of salidroside on intracellular free calcium concentration (([Ca^(2+)]i)), apoptosis, mitochondrial membrane potential (MMP) and activity during injury induced by hypoxia/hypoglycemia in cultured SH-SY5Y cells. METHODS: Mitochondrial activity was measured by methylthiazolyl tetrazolium test. MMP, [Ca^(2+)]i and apoptosis were measured by flow cytometry. RESULTS: SH-SY5Y cells were cultured in a hypoxia/hypoglycemia condition for 2, 4, 6 and 12 h, [Ca^(2+)]i and apoptosis rate significantly increased compared with control group (P<0.01). After hypoxia /hypoglycemia cultures, MMP and mitochondrial activity declined 29.17% ((P<0.01)) and 38.80% (P<0.01) at 2 h, 56.72% (P<0.01) and 63.58% (P<0.01) at 12 h, were lower than that in control group (P<0.01). Salidroside significantly decreased [Ca^(2+)]i and apoptosis rate, and increased MMP and mitochondrial activity in hypoxia /hypoglycemia-treated SH-SY5Y cells. CONCLUSIONS: Salidroside might inhibit the decline in MMP and mitochondrial activity induced by hypoxia /hypoglycemia, and has an inhibitory effects on neuronal apoptosis. The mechanism might be related to inhibiting intracellular calcium overload. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第7期1218-1221,共4页
Chinese Journal of Pathophysiology
