南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2013年
11期
1624-1627
,共4页
宋旭东%陈爱华%刘映峰%王先宝%周贻军%刘磊%张秀丽%王丽姿%杨平珍
宋旭東%陳愛華%劉映峰%王先寶%週貽軍%劉磊%張秀麗%王麗姿%楊平珍
송욱동%진애화%류영봉%왕선보%주이군%류뢰%장수려%왕려자%양평진
香芹酚%心脏%缺血再灌注损伤%氧化应激%凋亡
香芹酚%心髒%缺血再灌註損傷%氧化應激%凋亡
향근분%심장%결혈재관주손상%양화응격%조망
carvacrol%heart%ischemia-reperfusion injury%oxidative stress%apoptosis
目的：探索香芹酚（CAR）对小鼠心肌缺血再灌注损伤的作用及其相关机制。方法结扎雄性C57 BL/6小鼠冠状动脉左前降支45 min后解除结扎线构建急性心肌缺血再灌注（I-R）损伤模型。动物被随机分为5组：假手术组（n=13）、Vehicle组（DMSO in saline+I-R组）（n=13）、CAR组（CAR+I-R组）：分为20、40及60 mg/kg组（每组n=13）。CAR于缺血前15 min给药。缺血45 min再灌注2 h后检测心肌组织氧化应激水平及细胞凋亡率。结果同Vehicle组相比，CAR组心肌缺血再灌注后心肌梗死面积、氧化应激水平及细胞凋亡率显著降低（P<0.05）Vehicle组及CAR组DCFDA强度分别为（158.21±6.43）%及（123.47±9.82）%。Vehicle组及CAR组Mn-SOD活性分别为0.67±0.16及1.12±0.17 U/mg protein。Vehicle组及CAR组过氧化氢酶活性分别为0.14±0.09及0.63±0.07 U/mg protein。结论 CAR可通过降低氧化应激水平及心肌细胞凋亡率缓解小鼠心肌缺血再灌注损伤。
目的：探索香芹酚（CAR）對小鼠心肌缺血再灌註損傷的作用及其相關機製。方法結扎雄性C57 BL/6小鼠冠狀動脈左前降支45 min後解除結扎線構建急性心肌缺血再灌註（I-R）損傷模型。動物被隨機分為5組：假手術組（n=13）、Vehicle組（DMSO in saline+I-R組）（n=13）、CAR組（CAR+I-R組）：分為20、40及60 mg/kg組（每組n=13）。CAR于缺血前15 min給藥。缺血45 min再灌註2 h後檢測心肌組織氧化應激水平及細胞凋亡率。結果同Vehicle組相比，CAR組心肌缺血再灌註後心肌梗死麵積、氧化應激水平及細胞凋亡率顯著降低（P<0.05）Vehicle組及CAR組DCFDA彊度分彆為（158.21±6.43）%及（123.47±9.82）%。Vehicle組及CAR組Mn-SOD活性分彆為0.67±0.16及1.12±0.17 U/mg protein。Vehicle組及CAR組過氧化氫酶活性分彆為0.14±0.09及0.63±0.07 U/mg protein。結論 CAR可通過降低氧化應激水平及心肌細胞凋亡率緩解小鼠心肌缺血再灌註損傷。
목적：탐색향근분（CAR）대소서심기결혈재관주손상적작용급기상관궤제。방법결찰웅성C57 BL/6소서관상동맥좌전강지45 min후해제결찰선구건급성심기결혈재관주（I-R）손상모형。동물피수궤분위5조：가수술조（n=13）、Vehicle조（DMSO in saline+I-R조）（n=13）、CAR조（CAR+I-R조）：분위20、40급60 mg/kg조（매조n=13）。CAR우결혈전15 min급약。결혈45 min재관주2 h후검측심기조직양화응격수평급세포조망솔。결과동Vehicle조상비，CAR조심기결혈재관주후심기경사면적、양화응격수평급세포조망솔현저강저（P<0.05）Vehicle조급CAR조DCFDA강도분별위（158.21±6.43）%급（123.47±9.82）%。Vehicle조급CAR조Mn-SOD활성분별위0.67±0.16급1.12±0.17 U/mg protein。Vehicle조급CAR조과양화경매활성분별위0.14±0.09급0.63±0.07 U/mg protein。결론 CAR가통과강저양화응격수평급심기세포조망솔완해소서심기결혈재관주손상。
Objective To investigate the effect of carvacrol pretreatment on myocardial ischemia-reperfusion (I/R) injury and its underlying mechanisms. Methods Wild-type male C57 BL/6 mice were randomized into 5 groups (n=13), namely the sham-operated group, vehicle (DMSO in saline)+I/R group, carvacrol (20 mg/kg)+I/R group, carvacrol (40 mg/kg)+I/R group, and carvacrol (60 mg/kg)+I/R group. The mouse models of myocardial I/R injury were established by a 45-min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion for 2 h. Carvacrol or vehicle was administered intravenously 15 min before LAD occlusion. After reperfusion, the mice were examined for myocardial oxidative stress level and apoptosis rate. Results Compared with the vehicle group, the 3 carvacrol-pretreated groups showed significantly reduced myocardial infarct size, oxidative stress level and cardiac myocyte apoptosis rate (P<0.01). Conclusion Carvacrol can protect against myocardial I/R injury by inhibiting myocardial oxidative stress and apoptosis in mice.
