缺氧诱导因子1相关肽对化学缺氧引起的PC12细胞损伤的保护作用  

Protective effect of hypoxia-inducible factor-1 relevant peptide on chemical hypoxia-induced injury in PC12 cells

作　　者：严虹[1] 黄艳[1] 李华[1] 潘金顺[1] 王斌[1] 

机构地区：[1]南京医科大学药理学系,南京210029

出　　处：《中国新药杂志》2005年第4期429-432,共4页Chinese Journal of New Drugs

基　　金：国家自然科学青年基金(30000207);江苏省教育厅重点项目(KJB310001);江苏省高校高新技术产业化项目(JH01-050);南京医科大学科技发展基金(NY03065)

摘　　要：目的:研究氯化钴模拟化学缺氧条件下,缺氧诱导因子1相关肽(BW8)对PC12细胞损伤的影响。方法:氯化钴模拟缺氧后,给予不同浓度BW8,观察细胞生存率的变化,并测定细胞内谷胱苷肽(GSH)和超氧化物歧化酶(SOD)水平。结果:BW8可以抑制氯化钴诱导的PC12细胞存活率下降,且作用呈浓度依赖性;用尼莫地平预处理的PC12细胞存活率也显著提高,BW8的作用程度与尼莫地平接近;用终浓度为125μmol·L^(-1)的氯化钴处理细胞,可以显著降低细胞内GSH含量及SOD活力,而BW8可以浓度依赖性升高SOD活力,明显提高GSH含量。结论:多肽BW8对于化学缺氧引起的PC12细胞损伤具有一定的保护作用。Objective:To investigate the protective effect of the hypoxia-inducible factor-1 relevant peptide (BW8) on chemical hypoxia-induced injury in PC12 cells. Methods:The cell viability, glutathione (GSH) and superoxide dismutase (SOD) were assayed after PC12 cells were treated with CoCl_2 and peptide BW8 simultaneously. Results:CoCl_2 500μmol·L^(-1) could markedly reduce PC12 cell viability, while nimodipine 20μmol·L^(-1) significantly inhibited the reduction of cell viability evoked by CoCl_2. Peptide BW8 (0. 2μmol·L^(-1), 2μmol·L^(-1) and 20μmol·L^(-1) could concentration-dependently elevate the cell viability after CoCl_2 treatment. CoCl_2 125μmol·L(?)could significantly decrease GSH level and SOD activity. BW8 0. 2μmol·L^(-1) markedly suppress the inhibition of GSH induced by CoCl_2. SOD activity after CoCl_2 treatment was also increased by BW8 (0. 2μmol·L^(-1) and 2μmol·L^(-1)) in a concentration-dependent manner. Conclusion:Peptide BW8 could markedly inhibit the reduction of cell viability and GSH level and SOD activity induced by CoCl_2 in PC12 cell and might be effective in the prevention and treatment of neural injury.

关 键 词：相关肽 缺氧诱导因子1 化学缺氧 损伤 超氧化物歧化酶 谷胱苷肽 自由基 

分 类 号：R965.1[医药卫生—药理学] R743.31[医药卫生—药学]