中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2014年
38期
3024-3028
,共5页
赵悦%唐玉龙%索传涛%刘大一%李诗杨%黎辉
趙悅%唐玉龍%索傳濤%劉大一%李詩楊%黎輝
조열%당옥룡%색전도%류대일%리시양%려휘
氢%心肌缺血%再灌注损伤%内质网
氫%心肌缺血%再灌註損傷%內質網
경%심기결혈%재관주손상%내질망
Hydrogen%Myocardial ischemia%Reperfusion injury%Endoplasmic reticulum
目的 研究饱和氢盐水对大鼠心肌缺血再灌注损伤后心肌细胞内质网应激的影响.方法 选取健康成年清洁级雄性SD大鼠150只,采用随机数字表法将其分为5组(n=30):空白对照组(Ⅰ组)、假手术组(Ⅱ组)、缺血再灌注组(Ⅲ组)、饱和氢盐水治疗组(Ⅳ组)、生理盐水治疗组(Ⅴ组).Ⅰ组不做任何处理;Ⅱ组大鼠仅穿线不结扎;Ⅲ组制备大鼠心肌缺血再灌注损伤模型;Ⅳ组于再灌注前5 min给予1ml/100 g腹腔注射饱和氢生理盐水;Ⅴ组于再灌注前5 min给予1 ml/100 g腹腔注射等量生理盐水.于再灌注12、24 h后取左室心肌组织HE染色观察心肌病理学,同时采用原位末端转移酶标记法(TUNEL法)检测心肌细胞凋亡,蛋白质印迹法(Western blot)检测心肌细胞GRP78、Caspase-12、Bcl-2和Bax蛋白表达.结果 与Ⅰ组、Ⅱ组比较,Ⅲ组、Ⅳ组和Ⅴ组大鼠心肌缺血再灌注后心肌凋亡细胞增加,心肌细胞GRP78和Caspase-12表达水平升高,Bcl-2表达下调和Bax表达上调.与Ⅲ组、Ⅴ组比较,Ⅳ组大鼠心肌缺血再灌注后心肌凋亡细胞减少,心肌细胞GRP78和Caspase-12表达水平降低,Bcl-2表达上调和Bax表达下调.结论 饱和氢盐水可通过抑制内质网应激,降低细胞凋亡,减轻大鼠心肌缺血再灌注损伤,其机制可能与降低心肌细胞GRP78、Caspase-12和Bax蛋白表达,升高Bcl-2蛋白表达有关.
目的 研究飽和氫鹽水對大鼠心肌缺血再灌註損傷後心肌細胞內質網應激的影響.方法 選取健康成年清潔級雄性SD大鼠150隻,採用隨機數字錶法將其分為5組(n=30):空白對照組(Ⅰ組)、假手術組(Ⅱ組)、缺血再灌註組(Ⅲ組)、飽和氫鹽水治療組(Ⅳ組)、生理鹽水治療組(Ⅴ組).Ⅰ組不做任何處理;Ⅱ組大鼠僅穿線不結扎;Ⅲ組製備大鼠心肌缺血再灌註損傷模型;Ⅳ組于再灌註前5 min給予1ml/100 g腹腔註射飽和氫生理鹽水;Ⅴ組于再灌註前5 min給予1 ml/100 g腹腔註射等量生理鹽水.于再灌註12、24 h後取左室心肌組織HE染色觀察心肌病理學,同時採用原位末耑轉移酶標記法(TUNEL法)檢測心肌細胞凋亡,蛋白質印跡法(Western blot)檢測心肌細胞GRP78、Caspase-12、Bcl-2和Bax蛋白錶達.結果 與Ⅰ組、Ⅱ組比較,Ⅲ組、Ⅳ組和Ⅴ組大鼠心肌缺血再灌註後心肌凋亡細胞增加,心肌細胞GRP78和Caspase-12錶達水平升高,Bcl-2錶達下調和Bax錶達上調.與Ⅲ組、Ⅴ組比較,Ⅳ組大鼠心肌缺血再灌註後心肌凋亡細胞減少,心肌細胞GRP78和Caspase-12錶達水平降低,Bcl-2錶達上調和Bax錶達下調.結論 飽和氫鹽水可通過抑製內質網應激,降低細胞凋亡,減輕大鼠心肌缺血再灌註損傷,其機製可能與降低心肌細胞GRP78、Caspase-12和Bax蛋白錶達,升高Bcl-2蛋白錶達有關.
목적 연구포화경염수대대서심기결혈재관주손상후심기세포내질망응격적영향.방법 선취건강성년청길급웅성SD대서150지,채용수궤수자표법장기분위5조(n=30):공백대조조(Ⅰ조)、가수술조(Ⅱ조)、결혈재관주조(Ⅲ조)、포화경염수치료조(Ⅳ조)、생리염수치료조(Ⅴ조).Ⅰ조불주임하처리;Ⅱ조대서부천선불결찰;Ⅲ조제비대서심기결혈재관주손상모형;Ⅳ조우재관주전5 min급여1ml/100 g복강주사포화경생리염수;Ⅴ조우재관주전5 min급여1 ml/100 g복강주사등량생리염수.우재관주12、24 h후취좌실심기조직HE염색관찰심기병이학,동시채용원위말단전이매표기법(TUNEL법)검측심기세포조망,단백질인적법(Western blot)검측심기세포GRP78、Caspase-12、Bcl-2화Bax단백표체.결과 여Ⅰ조、Ⅱ조비교,Ⅲ조、Ⅳ조화Ⅴ조대서심기결혈재관주후심기조망세포증가,심기세포GRP78화Caspase-12표체수평승고,Bcl-2표체하조화Bax표체상조.여Ⅲ조、Ⅴ조비교,Ⅳ조대서심기결혈재관주후심기조망세포감소,심기세포GRP78화Caspase-12표체수평강저,Bcl-2표체상조화Bax표체하조.결론 포화경염수가통과억제내질망응격,강저세포조망,감경대서심기결혈재관주손상,기궤제가능여강저심기세포GRP78、Caspase-12화Bax단백표체,승고Bcl-2단백표체유관.
Objective To explore the effects of hydrogen-rich saline on endoplasmic reticulum stress during myocardial ischemia-reperfusion (I/R) in rats.Methods A total of 150 healthy male Sprague-Dawley rats were selected and then randomly divided into 5 groups of normal control (Ⅰ),sham operation (Ⅱ),myocardial ischemia-reperfusion (Ⅲ),hydrogen-rich saline (Ⅳ) and normal saline (Ⅴ)(n =30 each).Group Ⅰ had no treatment.In group Ⅱ,anterior descending branch was merely exposed but not ligated.Myocardial L/R was induced by an occlusion of anterior descending branch of left coronary artery for 30 min followed by 12 h and 24 h of reperfusion with bimbaum.Hydrogen-rich saline 1 ml/100 g was injected intraperitoneally 5 min before reperfusion in group Ⅳ.Normal saline 1 ml/100 g was injected intraperitoneally 5 min before reperfusion in group Ⅴ.The rats were sacrificed at 12 h and 24 h of reperfusion and heart tissues harvested.The pathological changes of myocardial tissue were detected by hematoxylin & eosin staining.The apoptotic cardiomyocytes of myocardial tissue were tested by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL).And the expressions of GRP78,Caspase-12,Bcl-2 and Bax in myocardial tissue were detected by Western blot.Results Compared with groups Ⅰ and Ⅱ,the numbers of apoptotic cardiomyocytes,the expression of GRP78,Caspase-12 and Bax in myocardial tissue significantly increased and the expression of Bcl-2 in myocardial tissue significantly decreased in groups Ⅲ,Ⅳ and Ⅴ.Compared with group Ⅲ and Ⅴ,the numbers of apoptotic cardiomyocytes,the expression of GRP78,Caspase-12 and Bax in myocardial tissue significantly decreased while the expression of Bcl-2 in myocardial tissue significantly increased in group Ⅳ.Conclusions Hydrogen-rich saline may decrease cell apoptosis and attenuate myocardial reperfusion injury through inhibiting endoplasmic reticulum stress.The mechanism may be associated with decreasing the expression of GRP78,Caspase-12 and Bax and increasing the expression of Bcl-2 in myocardial tissue.