摘要
目的 :研究预热应激对缺氧血管内皮细胞的保护作用及其发生机制 ,探索新的防治措施。方法 :将血管内皮细胞分为 :(1)缺氧组 ;(2 )热应激组 ;(3)预热应激 +缺氧组 ;(4)对照组。用全自动生化分析仪测定细胞培养液中乳酸脱氢酶 (LDH)活性 ,以台盼兰染色法测定细胞死亡率 ,用Griess化学法测定细胞培养液中NO-2 含量 ,以观察细胞NO生成量。结果 :缺氧血管内皮细胞LDH的释放量和细胞死亡率显著大于对照组 ,39℃预热应激可使其分别降低 2 9 47%和 33 6 7% ,41℃预热应激对缺氧细胞无明显保护作用。缺氧使血管内皮细胞NO生成量显著降低。39℃预热应激的缺氧血管内皮细胞NO生成量显著高于缺氧组 ,41℃预热应激的缺氧血管内皮细胞NO生成量显著低于对照及相应的缺氧组 ;血管内皮细胞NO生成量与细胞LDH释放量及细胞死亡率呈显著负相关。结论 :一定强度的预热应激可以对缺氧血管内皮细胞产生保护作用。
AIM: To observe the protective effect of heat stress preconditioning on endothelial cells under anoxia and explore its mechanism. METHODS: The endothelial cells were divided into 4 groups: (1) anoxia; (2) heat stress; (3) heat stress preconditioning + hypoxia; (4) control. LDH activity was measrued by using Automatic Biochemistry Analysis-Meter. Cell death rate was determined by trypan blue, NO production was tested by measuring NO - 2/NO - 3 content in cellular culture medium by using Griess assay. RESULTS: LDH release and cell death rate of the anoxia endothelial cells significantly increased compared with control; 39℃ heat stress preconditioning reduced those increment by 29、47%, 33.67% respectively. 41℃ heat stress preconditioning has no protection against the anoxia-induced injury in endothelial cells. The NO production in anoxic endothelial cells decreased markedly. 39℃ heat stress preconditioning induced the increase in NO production in endothelial cells, but 41℃ heat stress preconditioning made the NOS activity decrease. The NO production was correlated negatively with LDH release and cell death rate in anoxic endothelial cells. CONCLUSION: The heat stress preconditioning within the limits can protect the endothelial cells from anoxia injury. The increase in NO in endothelial cells may play an important role in the mechanism of the protective effect.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第9期904-907,共4页
Chinese Journal of Pathophysiology
