文章摘要
张洁心,刘剑南,陆 甘,杨 笛,殷国勇.N-乙酰半胱氨酸在慢性间歇缺氧小鼠心肌损伤中的作用研究[J].南京医科大学学报,2009,29(8):1059~1062
N-乙酰半胱氨酸在慢性间歇缺氧小鼠心肌损伤中的作用研究
The effect of N-acetylcysteine on cardiocytes injury in mouse exposed to chronic intermittent hypoxia
投稿时间:2009-04-07  
DOI:10.7655
中文关键词: 阻塞性睡眠呼吸暂停  慢性间歇缺氧  氧化应激  N-乙酰半胱氨酸
英文关键词: obstructive sleep apnea syndrome  chronic intermittent hypoxia  oxidative stress  N-acetylcysteine
基金项目:江苏省大学生实践创新训练计划立项建设项目(2007012)
作者单位
张洁心 南京医科大学第一临床医学院,江苏 南京 210029 
刘剑南 江苏省老年医院呼吸科,江苏 南京 210024 
陆 甘 江苏省老年医院呼吸科,江苏 南京 210024 
杨 笛 南京医科大学第一附属医院心血管研究所,江苏 南京 210029 
殷国勇 南京医科大学第一附属医院骨科,江苏 南京 210029 
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中文摘要:
      目的:通过建立慢性间歇缺氧(CIH)模拟阻塞性睡眠呼吸暂停(OSAS)的动物模型,观察CIH对心脏的损伤及其可能的作用机制?方法:ICR鼠33只随机分成3组:慢性间歇缺氧组?N-乙酰半胱氨酸干预组?对照组?硫代巴比妥酸(TBA)法和黄嘌呤氧化酶法分别检测3组实验鼠心肌匀浆中丙二醛(MDA)?超氧化物歧化酶(SOD)在N-乙酰半胱氨酸干预前后的变化?酶联免疫法检测3组鼠血清中心肌肌钙蛋白I(cTnI)水平?结果:① 慢性间歇缺氧组SOD活性及MDA水平高于对照组和N-乙酰半胱氨酸干预组(P < 0.05),N-乙酰半胱氨酸干预组MDA水平低于对照组(P < 0.01);②慢性间歇缺氧组及N-乙酰半胱氨酸干预组cTnI均高于对照组(P < 0.01);③组织病理切片结果表明慢性间歇缺氧组及N-乙酰半胱氨酸干预组心肌组织变性,横纹模糊,伴有纤维性渗出物,而对照组正常?结论:OSAS通过氧化应激产生的过量活性氧造成心肌损伤,给予N-乙酰半胱氨酸干预后可部分抑制这种损伤?
英文摘要:
      Objective:To study the effect of N-acetylcysteine(NAC)on cardiocytes injury induced by chronic intermittent hypoxia (CIH) by establishing an animal model of obstructive sleep apnea syndrome(OSAS). Methods:Thirty-three ICR mouse were divided into 3 groups randomly:control,CIH and NAC groups. Malondialdehyde(MDA) and superoxide dismutase(SOD) in the cardiocyte homogenates were measured before and after the treatment of NAC using thiobarbituric acid(TBA) and xanthine oxidase methods respectively. In addition,the concentration of cardiac troponin I(cTnI) in the serum was detected by ELISA. Results:① The SOD activity and MDA concentration of CIH group were significantly higher than those of other groups(P < 0.05). The MDA concentration of NAC group was lower than that of control group(P < 0.01). ② The cTnI concentration of CIH and NAC groups was significantly higher than that of control group(P < 0.01). ③The degeneration of muscular tissues,transverse striation blurred,and fabric effusion were observed in tissue pathological section in CIH and NAC groups. However,normal tissue was found in control group. Conclusion:The cardiocytes were injuried by producing activation oxygen in OSAS animals,and this effect can be partially inhibited by NAC.
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