中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2014年
11期
1216-1219
,共4页
王卉%田建立%张蕴%王林
王卉%田建立%張蘊%王林
왕훼%전건립%장온%왕림
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
睡眠呼吸暫停綜閤徵%半胱氨痠天鼕氨痠蛋白酶3%過氧化物酶%細胞凋亡
수면호흡잠정종합정%반광안산천동안산단백매3%과양화물매%세포조망
Sleep apnea syndromes%Caspase 3%Peroxidase%Apoptosis
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.
目的 通過觀察慢性間歇低氧對高脂餵養大鼠心肌細胞組織病理學、氧化應激和細胞凋亡指標影響,探討慢性間歇低氧誘導的心肌細胞損傷可能的髮病機製. 方法 24隻雄性Wistar大鼠隨機均分為3組,空白對照組大鼠採用普通鼠料餵養,高脂組採用高脂飼料餵養,高脂+間歇低氧組採用高脂飼料餵養,同時給予7 h/d間歇低氧處理.觀察3組大鼠9週末心肌組織病理學、心肌細胞超微結構變化,心肌組織凋亡調控因子天鼕氨痠特異性半胱氨痠蛋白酶3 (Caspase-3)和氧化應激指標髓過氧化物酶(MPO)活性變化. 結果 空白對照組8隻大鼠心肌Caspase-3、MPO酶活性分彆為0.21±0.06、3.20±0.58,高脂組8隻大鼠分彆為0.80±0.11、10.87±1.96,高脂+間歇低氧組7隻大鼠分彆為1.15±0.21、13.17±2.22,差異有統計學意義(F=89.94、71.24,均P=0.001);高脂組、高脂+間歇低氧組心肌Caspase-3、MPO酶活性明顯高于空白對照組(均P<0.01),而高脂+間歇低氧組心肌Caspase-3、MPO酶活性明顯高于高脂組(均P<0.05).光鏡結果顯示,空白對照組大鼠心肌結構未見異常,高脂組心肌細胞齣現多種病理損害,高脂+間歇低氧組心肌細胞損傷更為明顯. 結論 慢性間歇低氧伴高脂複閤條件對心肌細胞病理損傷較單純高脂組更為明顯,氧化應激誘導的細胞凋亡可能在其髮病機製中起重要作用.
목적 통과관찰만성간헐저양대고지위양대서심기세포조직병이학、양화응격화세포조망지표영향,탐토만성간헐저양유도적심기세포손상가능적발병궤제. 방법 24지웅성Wistar대서수궤균분위3조,공백대조조대서채용보통서료위양,고지조채용고지사료위양,고지+간헐저양조채용고지사료위양,동시급여7 h/d간헐저양처리.관찰3조대서9주말심기조직병이학、심기세포초미결구변화,심기조직조망조공인자천동안산특이성반광안산단백매3 (Caspase-3)화양화응격지표수과양화물매(MPO)활성변화. 결과 공백대조조8지대서심기Caspase-3、MPO매활성분별위0.21±0.06、3.20±0.58,고지조8지대서분별위0.80±0.11、10.87±1.96,고지+간헐저양조7지대서분별위1.15±0.21、13.17±2.22,차이유통계학의의(F=89.94、71.24,균P=0.001);고지조、고지+간헐저양조심기Caspase-3、MPO매활성명현고우공백대조조(균P<0.01),이고지+간헐저양조심기Caspase-3、MPO매활성명현고우고지조(균P<0.05).광경결과현시,공백대조조대서심기결구미견이상,고지조심기세포출현다충병리손해,고지+간헐저양조심기세포손상경위명현. 결론 만성간헐저양반고지복합조건대심기세포병리손상교단순고지조경위명현,양화응격유도적세포조망가능재기발병궤제중기중요작용.
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.