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中华眼镜蛇毒组分F/H对大鼠心肌细胞缺氧-再给氧损伤的作用探讨
引用本文:侯力强,何泉华,江中喜,赵路宁,孔天翰,管锦霞.中华眼镜蛇毒组分F/H对大鼠心肌细胞缺氧-再给氧损伤的作用探讨[J].海峡药学,2004,16(1):39-41.
作者姓名:侯力强  何泉华  江中喜  赵路宁  孔天翰  管锦霞
作者单位:广州医学院蛇毒研究所,广州,510182;广州医学院第二附属医院,广州,510260
基金项目:广东省医学科学技术研究基金 (课题号 B19990 75、B2 0 0 0 0 67),广东省自然科学基金博士启动基金 (课题号 9944 0 9)资助
摘    要:以Laarse方法建立大鼠心肌细胞缺氧-再给氧模型.缺氧缺糖60min.再给氧1h.探讨组份F和H对实验性心肌细胞缺血再灌注的保护作用。实验结果显示,缺氧后心肌细胞成活率显著减少,心肌释放LDH含量显著增加.细胞膜流动性下降,缺氧再给氧后上述各指标改变加剧。组份F和H能明显提高心肌细胞成活率,减少LDH的释放.增加细胞膜流动性.减少心肌细胞膜的损伤,实验结论,组份F和H有明显抗心肌细胞缺氧-再给氧损伤的作用,尤以组份F作用更显著。

关 键 词:眼镜蛇  抗氧化  心肌细胞  乳酸脱氢酶
文章编号:1006-3765(2004)01-0039-03

Rearch on the Effect of Fraction F/H from Naja naja atra Venom on Myocytes Anoxia-Reoxygenation Injures in Rats
HOU Li-qiang ,HE Quan-hua ,JIANG Zhong-xi ,ZHAO Lu-ning ,KONG Tian-han ,GUAN Jin-xia.Rearch on the Effect of Fraction F/H from Naja naja atra Venom on Myocytes Anoxia-Reoxygenation Injures in Rats[J].Strait Pharmaceutical Journal,2004,16(1):39-41.
Authors:HOU Li-qiang  HE Quan-hua  JIANG Zhong-xi  ZHAO Lu-ning  KONG Tian-han  GUAN Jin-xia
Institution:HOU Li-qiang 1,HE Quan-hua 1,JIANG Zhong-xi 2,ZHAO Lu-ning 1,KONG Tian-han 1,GUAN Jin-xia 1
Abstract:According to Laarse's method,the anoxia-reoxygenation model of cultured rats myocardial cells was developed;anoxia and glucose deficiency for 60min followed by reoxygenation and re-exposure to glucose for 1h,in order to research on the protective effect of Fraction F/H isolated from Naja naja atra venom on experimental myocytes anoxia-reoxygenation injuries.The results showed that the survival rate of myocardial cells in the anoxia group was significantly decreased,release of lactate dehydrogenase(LDH)from myocytes was increased and membrane fluidity was decreased,all the changes were much more severe in the anoxia-reoxygenation group.Fraction F/H increased the survival rate of myocardial cells and membrane fluidity,decreased the release of LDH.These results suggested that Fraction F/H may provide obvious protective effects on the anoxia-reoxygenation damages on myocardium.
Keywords:Naja naja atra  Antioxidation  Myocytes  LDH
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