中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
7期
2972-2976
,共5页
赵航天%陈学颖%范凡%刘湘玮%王聪%申程%马鑫%朱洪%孙爱军%葛均波
趙航天%陳學穎%範凡%劉湘瑋%王聰%申程%馬鑫%硃洪%孫愛軍%葛均波
조항천%진학영%범범%류상위%왕총%신정%마흠%주홍%손애군%갈균파
再灌注损伤%内质网%应激%细胞凋亡%解酒药%乙醛脱氢酶2
再灌註損傷%內質網%應激%細胞凋亡%解酒藥%乙醛脫氫酶2
재관주손상%내질망%응격%세포조망%해주약%을철탈경매2
Reperfusion injury%Endoplasmic reticulum%Stress%Apoptosis%Hangover medicine%Aldehyde dehydrogenase 2
目的通过大鼠心肌缺血再灌注模型研究解酒药对缺血再灌注（ IR ）损伤的保护作用。方法雄性SD大鼠分为IR＋生理盐水对照组、IR＋解酒药组、IR＋解酒药＋cyanamide （乙醛脱氢酶2抑制剂，氨基氰，CH2N2）组。伊文思蓝和TTC染色评估心肌梗死面积，TUNEL法测定缺血再灌注区域心肌细胞凋亡情况，Western blot测定分析内质网应激相关蛋白Grp78和Chop含量变化以及凋亡相关蛋白Caspase12含量变化。结果解酒药减轻心肌梗死面积，而cyanamide的加入部分抵消了解酒药对心肌缺血再灌注的保护作用[IR＋生理盐水对照组：（57.72±6.52）％；IR＋解酒药组：（35.59±5.77）％；IR＋解酒药＋cyanamide组：（46.83±5.96）％；IR＋生理盐水对照组vs．IR＋解酒药组，P＜0.01；IR＋生理盐水对照组vs．IR＋解酒药＋cyanamide组，P＜0.01；IR＋解酒药组vs．IR＋解酒药＋cyanamide组，P＜0.01]。 Grp78、Chop、Caspase12蛋白水平于IR＋生理盐水对照组、IR＋解酒药组、IR＋解酒药＋cyanamide 组中均无统计学差异（ P＞0.05）。结论在心肌缺血再灌注损伤早期，解酒药对心肌缺血再灌注损伤具有保护作用，且抑制ALDH2后此作用消失，但其机制可能不是通过调控ALDH2参与的内质网应激而实现的。
目的通過大鼠心肌缺血再灌註模型研究解酒藥對缺血再灌註（ IR ）損傷的保護作用。方法雄性SD大鼠分為IR＋生理鹽水對照組、IR＋解酒藥組、IR＋解酒藥＋cyanamide （乙醛脫氫酶2抑製劑，氨基氰，CH2N2）組。伊文思藍和TTC染色評估心肌梗死麵積，TUNEL法測定缺血再灌註區域心肌細胞凋亡情況，Western blot測定分析內質網應激相關蛋白Grp78和Chop含量變化以及凋亡相關蛋白Caspase12含量變化。結果解酒藥減輕心肌梗死麵積，而cyanamide的加入部分牴消瞭解酒藥對心肌缺血再灌註的保護作用[IR＋生理鹽水對照組：（57.72±6.52）％；IR＋解酒藥組：（35.59±5.77）％；IR＋解酒藥＋cyanamide組：（46.83±5.96）％；IR＋生理鹽水對照組vs．IR＋解酒藥組，P＜0.01；IR＋生理鹽水對照組vs．IR＋解酒藥＋cyanamide組，P＜0.01；IR＋解酒藥組vs．IR＋解酒藥＋cyanamide組，P＜0.01]。 Grp78、Chop、Caspase12蛋白水平于IR＋生理鹽水對照組、IR＋解酒藥組、IR＋解酒藥＋cyanamide 組中均無統計學差異（ P＞0.05）。結論在心肌缺血再灌註損傷早期，解酒藥對心肌缺血再灌註損傷具有保護作用，且抑製ALDH2後此作用消失，但其機製可能不是通過調控ALDH2參與的內質網應激而實現的。
목적통과대서심기결혈재관주모형연구해주약대결혈재관주（ IR ）손상적보호작용。방법웅성SD대서분위IR＋생리염수대조조、IR＋해주약조、IR＋해주약＋cyanamide （을철탈경매2억제제，안기청，CH2N2）조。이문사람화TTC염색평고심기경사면적，TUNEL법측정결혈재관주구역심기세포조망정황，Western blot측정분석내질망응격상관단백Grp78화Chop함량변화이급조망상관단백Caspase12함량변화。결과해주약감경심기경사면적，이cyanamide적가입부분저소료해주약대심기결혈재관주적보호작용[IR＋생리염수대조조：（57.72±6.52）％；IR＋해주약조：（35.59±5.77）％；IR＋해주약＋cyanamide조：（46.83±5.96）％；IR＋생리염수대조조vs．IR＋해주약조，P＜0.01；IR＋생리염수대조조vs．IR＋해주약＋cyanamide조，P＜0.01；IR＋해주약조vs．IR＋해주약＋cyanamide조，P＜0.01]。 Grp78、Chop、Caspase12단백수평우IR＋생리염수대조조、IR＋해주약조、IR＋해주약＋cyanamide 조중균무통계학차이（ P＞0.05）。결론재심기결혈재관주손상조기，해주약대심기결혈재관주손상구유보호작용，차억제ALDH2후차작용소실，단기궤제가능불시통과조공ALDH2삼여적내질망응격이실현적。
Objective To investigate whether hangover medicine plays cardioprotective role in the rat model of myocardial ischemia-reperfusion injury , and to reveal the possible mechanism .Methods 200-250 g Sprague-Dawley rats were divided into 3 groups randomly,before myocardial ischemia and reperfusion procedure ,saline(n=6),hangover medicine (n =6) or hangover medicine +cyanamide were given respectively by oral gavage and intraperitoneal injection .Myocardial infarction ratio was calculated by Evans blue and triphenyltetrazolium chloride (TTC) staining, and myocardial apoptosis was evaluated by TUNEL assay .Expression of endoplasmic-reticulum-stress-related proteins ( Grp78 , Chop ) and apoptosis-related protein ( Caspase12 ) were quantified by Western blot . Results The infarction size was significantly reduced by the treatment of hangover medicine [ hangover medicine group vs.saline group,(35.59 ±5.77)%vs.(57.72 ±6.52)%,P<0.01].However,when the hangover medicine was blocked,the protection was diminished [hangover medicine group vs.hangover medicine and cyanamide group , (35.59 ±5.77)% vs.(46.83 ±5.96)%,P <0.01].Myocardial apoptosis and the levels of Grp78,Chop, Caspase12 were not significantly different between the three groups ( P>0.05 ) .Conclusions In the early phase of myocardial ischemia and reperfusion injury ,hangover medicine provides myocardial protection ,which can be blocked by ALDH2 inhibitor.This influence may not be implicated through ALDH 2 initiated endoplasmic reticulum stress .
