机构地区:[1]天津医科大学总医院保健医疗部天津市老年病学研究所,300052 [2]天津医科大学第二医院
出 处:《中华老年医学杂志》2014年第11期1216-1219,共4页Chinese Journal of Geriatrics
摘 要:目的 通过观察慢性间歇低氧对高脂喂养大鼠心肌细胞组织病理学、氧化应激和细胞凋亡指标影响,探讨慢性间歇低氧诱导的心肌细胞损伤可能的发病机制. 方法 24只雄性Wistar大鼠随机均分为3组,空白对照组大鼠采用普通鼠料喂养,高脂组采用高脂饲料喂养,高脂+间歇低氧组采用高脂饲料喂养,同时给予7 h/d间歇低氧处理.观察3组大鼠9周末心肌组织病理学、心肌细胞超微结构变化,心肌组织凋亡调控因子天冬氨酸特异性半胱氨酸蛋白酶3 (Caspase-3)和氧化应激指标髓过氧化物酶(MPO)活性变化. 结果 空白对照组8只大鼠心肌Caspase-3、MPO酶活性分别为0.21±0.06、3.20±0.58,高脂组8只大鼠分别为0.80±0.11、10.87±1.96,高脂+间歇低氧组7只大鼠分别为1.15±0.21、13.17±2.22,差异有统计学意义(F=89.94、71.24,均P=0.001);高脂组、高脂+间歇低氧组心肌Caspase-3、MPO酶活性明显高于空白对照组(均P<0.01),而高脂+间歇低氧组心肌Caspase-3、MPO酶活性明显高于高脂组(均P<0.05).光镜结果显示,空白对照组大鼠心肌结构未见异常,高脂组心肌细胞出现多种病理损害,高脂+间歇低氧组心肌细胞损伤更为明显. 结论 慢性间歇低氧伴高脂复合条件对心肌细胞病理损伤较单纯高脂组更为明显,氧化应激诱导的细胞凋亡可能在其发病机制中起重要作用.Objective To investigate the effect of chronic intermittent hypoxia (CIH) on myocardial tissue pathology,oxidative stress and apoptosis in rat fed a high-fat diet,and to explore the possible mechanism of CIH induced cardiomyocyte injury.Methods A total of 24 male Wistar rats were randomly divided into 3 groups (n=8 each).The control group was fed common rat forage,the high-fat group was fed high-fat forage,and the high-fat plus intermittent hypoxia group was fed high-fat forage combined with a 7h/d intermittent hypoxia treatment.The changes of myocardial tissue pathology and ultrastructure of cardiomyocyte,and the activities of apoptosis regulating factor cysteine-containing aspartate-specific proteases-3 (caspase-3) and oxidative stress marker myeloperoxidase (MPO) were observed in the 3 groups after 4 weeks of treatment.Results There were significant differences in the activities of caspase-3 and MPO among the three group (F=89.94,71.24,both P=0.001).The activities of caspase-3 and MPO were lower in the control group than in the high-fat group and in high fat plus intermittent hypoxia group [(0.21±0.06) vs.(0.80±0.11),(1.15±0.21),(3.20±0.58) vs.(10.87±1.96),(13.17±2.22),P<0.01].The activities of caspase-3 and MPO were higher in the high-fat plus intermittent hypoxia group than in the high fat group[(1.15±0.21) vs.(0.80±0.11),(13.17±2.22) vs.(10.87±1.96),P<0.01].No abnormal findings in the structure of cardiomyocyte were observed in the control group,while multiple pathologic damages in cardiomyocyte were detected in the high-fat group,and more obvious injuries in the high-fat plus intermittent hypoxia group.Conclusions The pathologic damages to cardiomyocyte are more serious in high fat and intermittent hypoxia group than in the high-fat group.Apoptosis induced by oxidative stress may play an important role in the pathogenesis of these injuries.
关 键 词:睡眠呼吸暂停综合征 半胱氨酸天冬氨酸蛋白酶3 过氧化物酶 细胞凋亡
分 类 号:R766[医药卫生—耳鼻咽喉科]
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