目的:探讨缩醛基毛冬青提取化合物R4对缺氧/复氧损伤心肌细胞的保护作用及其机制.方法:采用原代培养的新生大鼠心肌细胞建立缺氧/复氧损伤模型,实验分为正常细胞培养组和缺氧/复氧损伤模型组、缺氧/复氧损伤+缩醛基毛冬青提取化合物R4(5、10、20 μmol/L)组和缺氧/复氧损伤+ verapamil(5 μmol/L)组.用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)的活性,硫代巴比妥酸显色法测定丙二醛(MDA)含量,MTT染色法测定线粒体脱氢酶活性改变,化学比色法测定乳酸脱氢酶(LDH)活性变化,Griess法测定一氧化氮(NO)的含量.结果:缩醛基毛冬青提取化合物R4可显著提高缺氧/复氧损伤心肌细胞内SOD的活性及细胞内线粒体脱氢酶活性,能显著抑制LDH的活性、MDA的生成以及提高NO的含量,并能明显抑制心肌细胞凋亡.结论:缩醛基毛冬青提取化合物R4具有明显抗缺氧/复氧损伤、保护心肌细胞的作用.%AIM:To observe the effects of acetal hairy holly extractive compound R4( AHHECR4) on myocardial cell injury induced by hypoxia/reoxygenation. METHODS: The model of rat myocardial cell injury was induced by hypoxia/reoxygenation. The activity of superoxide dismutase ( SOD) in the myocardial cells was measured by the method of xanthine oxidase. The content of malondialdehyde (MDA) was determined by the method of thiobarbituric acid. The activity of dehydrogenase (A) in mitochondria was detected by MTT assay. The activity of lactate dehydrogenase( LDH) and the content of NO in the culture medium were also evaluated. RESULTS; AHHECR4 at concentrations of 5, 10 and 20 μmol/ L remarkably increased SOD activity and the value of A, and significantly inhibited MDA production and LDH leakage. Greatly increased content of NO in the culture medium was also observed. CONCLUSION; The results indicate that AHHECR4 has a protective effect on myocardial cells under the condition of hypoxia/reoxygenation injury.
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