实用医学杂志
實用醫學雜誌
실용의학잡지
The Journal of Practical Medicine
2015年
17期
2796-2798
,共3页
缺血再灌注损伤%线粒体%氧化磷酸化
缺血再灌註損傷%線粒體%氧化燐痠化
결혈재관주손상%선립체%양화린산화
Ischemia and reperfusion injury%Mitochondria%Oxidative phosphorylation
目的：探讨小鼠心肌缺血再灌注早期线粒体呼吸链复合体氧化磷酸化功能变化。方法：40只C57BL／6小鼠随机分组为：空白对照组（TC组）、缺血＋再灌注5 min组（IR 5 min组）、缺血＋再灌注10 min （IR 10 min组）组、缺血＋再灌注15 min组（IR 15 min组）、缺血＋再灌注30 min组（IR 30 min组），每组8只，采用小鼠Langendorff模型，TC组给予平衡灌注45 min；缺血再灌注组均给予缺血25 min，随后给予5、10、15和30 min的再灌注。提取心肌线粒体，测定不同线粒体呼吸链复合体的呼吸功能变化。结果：与TC组相比，IR 5 min组以谷氨酸＋苹果酸为底物的复合体Ⅰ呼吸功能无明显改变，而IR 10 min、15 min和30 min组，复合体Ⅰ的呼吸功能显著抑制；与TC组相比，以琥珀酸、TMPD／ascobate为底物的复合体Ⅱ、Ⅳ的呼吸功能在IR 5 min组即开始下降，且随再灌注时间延长呼吸功能抑制程度加重。结论：小鼠心肌缺血再灌注早期线粒体呼吸链复合体的氧化磷酸化功能随再灌注时间延长存在不同变化，研究不同线粒体复合体在缺血再灌注损伤中的作用，应选择不同的缺血后再灌注时间。
目的：探討小鼠心肌缺血再灌註早期線粒體呼吸鏈複閤體氧化燐痠化功能變化。方法：40隻C57BL／6小鼠隨機分組為：空白對照組（TC組）、缺血＋再灌註5 min組（IR 5 min組）、缺血＋再灌註10 min （IR 10 min組）組、缺血＋再灌註15 min組（IR 15 min組）、缺血＋再灌註30 min組（IR 30 min組），每組8隻，採用小鼠Langendorff模型，TC組給予平衡灌註45 min；缺血再灌註組均給予缺血25 min，隨後給予5、10、15和30 min的再灌註。提取心肌線粒體，測定不同線粒體呼吸鏈複閤體的呼吸功能變化。結果：與TC組相比，IR 5 min組以穀氨痠＋蘋果痠為底物的複閤體Ⅰ呼吸功能無明顯改變，而IR 10 min、15 min和30 min組，複閤體Ⅰ的呼吸功能顯著抑製；與TC組相比，以琥珀痠、TMPD／ascobate為底物的複閤體Ⅱ、Ⅳ的呼吸功能在IR 5 min組即開始下降，且隨再灌註時間延長呼吸功能抑製程度加重。結論：小鼠心肌缺血再灌註早期線粒體呼吸鏈複閤體的氧化燐痠化功能隨再灌註時間延長存在不同變化，研究不同線粒體複閤體在缺血再灌註損傷中的作用，應選擇不同的缺血後再灌註時間。
목적：탐토소서심기결혈재관주조기선립체호흡련복합체양화린산화공능변화。방법：40지C57BL／6소서수궤분조위：공백대조조（TC조）、결혈＋재관주5 min조（IR 5 min조）、결혈＋재관주10 min （IR 10 min조）조、결혈＋재관주15 min조（IR 15 min조）、결혈＋재관주30 min조（IR 30 min조），매조8지，채용소서Langendorff모형，TC조급여평형관주45 min；결혈재관주조균급여결혈25 min，수후급여5、10、15화30 min적재관주。제취심기선립체，측정불동선립체호흡련복합체적호흡공능변화。결과：여TC조상비，IR 5 min조이곡안산＋평과산위저물적복합체Ⅰ호흡공능무명현개변，이IR 10 min、15 min화30 min조，복합체Ⅰ적호흡공능현저억제；여TC조상비，이호박산、TMPD／ascobate위저물적복합체Ⅱ、Ⅳ적호흡공능재IR 5 min조즉개시하강，차수재관주시간연장호흡공능억제정도가중。결론：소서심기결혈재관주조기선립체호흡련복합체적양화린산화공능수재관주시간연장존재불동변화，연구불동선립체복합체재결혈재관주손상중적작용，응선택불동적결혈후재관주시간。
Objective To investigate the alternation of mitochondrial oxidative phosphorylation post-ischemia/reperfusion myocardial injury in mice. Methods The C57BL/6 mice were randomly divided into five groups. The mouse hearts in the time control group (TC) were perfused for 45 min in identical Krebs-Henseleit buffer without any treatment. In the ischemia/reperfusion groups, the mouse hearts were treated with different reperfusion time including 5, 10, 15 or 30 min, following by the same ischemia period of 25 min. The mitochondria were extracted from the left ventricular post-reperfusion. The respiratory function including R3, R4, RCR, and the maximal rate of state 3 respiration (2 mmol/L ADP) were measured. Results The R3, RCR and P/O of mitochondria, using glutamate + malate as substrates, were decreased significantly at 10 min, 15 min and 30 min post-ischemia/reperfusion (P < 0.05, respectively), but not in the 5-min-reperfusion group compared with the time control group. And the respiratory function, using succinate, and TMPD-ascorbate as substrates, decreased significantly in different ischemia/reperfusion groups compared with the time control (P < 0.05, respectively). Conclusions The mitochondrial respiratory function changes differently in different complex at the early stage of reperfusion after ischemia. So different ischemia/reperfusion time should be chosen to detect the alternations of different mitochondrial complex after heart injury.
