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卡托普利对外源性羟自由基诱导心肌细胞凋亡的影响 被引量:1

The effect of captopril on apoptosis of neonatal rat cardiomyocytes induced by exogenous hydroxyl free radical
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摘要 目的 观察卡托普利对由外源性羟自由基诱导的心肌细胞凋亡有无影响。方法 ①利用第 4代心肌细胞 ,随机分成 15组 ,在终浓度为 10 -5mol/L、10 -4 mol/L、10 -3mol/L、10 -2 mol/L、10 -1mol/L的羟自由基无血清条件培养下分别共孵育 8h、16h、2 4h ,确定 10 -3 mol/L及 2 4h为诱导心肌细胞凋亡的最佳浓度及时间。②在上述条件下分别观察 3种不同浓度卡托普利 (10 -7mol/L、10 -6mol/L、10 -5mol/L)对心肌细胞存活率、形态学、DNA琼脂糖凝胶电泳及培养液中血管紧张素Ⅰ转换酶 (angiotensin convertingenzyme ,ACE)活性等参数的影响。结果 ①随着外源性羟自由基浓度升高、心肌细胞存活率明显降低 ,在外源性羟自由基终浓度为 10 -5~10 -3 mol/L范围内 ,随着浓度升高 ,培养液中ACE活性逐渐升高 ,但高于 10 -3 mol/L浓度时反而降低。② 10 -3 mol/L作用心肌细胞 2 4h心肌细胞凋亡程度最明显 ,在此条件下 ,加用卡托普利 (10 -7mol/L、10 -6mol/L、10 -5mol/L) ,心肌细胞存活率明显升高 ,培养液中ACE活性降低 ,心肌细胞凋亡程度降低 ,呈剂量依赖性。结论 卡托普利能减轻由外源性羟自由基诱导的乳鼠心肌细胞凋亡。 Objective To observe the effect of captopril on apoptosis of neonatal rat cardiomyocytes (NRCs) induced by exogenous hydroxyl free radical (EHFR). Methods ①The fouth passage of NRCs were divided randomly into fifteen groups and were cultured with EHFR(10 -5 mol/L、10 -4 mol/L、10 -3 mol/L、10 -2 mol/L、10 -1 mol/L) in free-serum medium for 8hr\, 16hr and 24hr respectly in order to ditermine the best concentration of EHFR and culture time inducing apoptosis. ②Under 10 -3 mol/L EHFR condition, NRCs were co-cultured with three end concentrations of captopril (10 -7 mol/L、10 -6 mol/L、10 -5 mol/L). The survival rate and morphology of NRCs\, activity of angioteasin converting enzyme (ACE) in medium DNA ladder and percentage of NRCs with positive reaction in nuclei by the terminal deoxynucleotidyl transferase were evaluated. Result ①The survival rate of NRCs significantly decreased as the concentration of EHFR increased. The activity of ACE in medium increased as the concentration EHFR increased within the arrange of 10 -5 ~10 -3 mol/L, but it decreased when the concentration of EHFR was beyond 10 -3 mol/L. ② The most obvious apoptosis of NRCs was found at the concentration of 10 -3 mol/L EHFR for 24hr culture. Under this culture condition, captopril significantly increased the survival rate of NRCs, decreased the activity of ACE in medium and attenuated apoptosis of NRCs in a dose dependent fashion. Conclusion Captopril attenuates the apoptosis of NRCs induced by EHFR.
出处 《岭南心血管病杂志》 2000年第1期49-54,共6页 South China Journal of Cardiovascular Diseases
关键词 心肌细胞 细胞凋亡 羟自由基 卡托普利 Cardiomyocytes Apoptosis Hydroxyl free radical Captopril
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  • 1刘智峰,方允中.血液中超氧化物歧化酶测定的光化学扩增法[J]军事医学科学院院刊,1986(04).

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  • 1Linz W,J Cardiovase Pharmacol,1993年,22卷,Suppl期,S1页
  • 2刘建华,第二军医大学学报,1987年,8卷,5期,367页

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