CAJ | 학술논문

目的通过建立大鼠心肌缺血预处理(IPC)模型及心肌梗死模型,探讨IPC对心肌的保护作用及其对脂联素表达的影响.方法成年大鼠(4月龄)建立IPC模型及IPC后心肌梗死模型,随机分为空白对照组(0、6、12和24 h亚组)、IPC组(0、6、12和24 h亚组)、单纯心肌梗死(MI)组及IPC+MI组.采用Masson三色染色法测量心肌梗死面积(乳头肌平面梗死心肌与左心室心肌面积的比值,%),免疫组织化学法和实时荧光定量PCR法检测脂联素在心肌组织中的蛋白和mRNA表达水平,利用大鼠血浆标本做酶联免疫吸附实验,观察循环中脂联素含量的变化.结果 IPC+MI组大鼠心肌梗死面积明显小于MI组[(20±2)%比(31±3)%,P＜0.05＝.IPC组6和12 h亚组大鼠心肌组织中脂联素mRNA的表达分别是空白对照组相应时间点亚组的2.2倍和2.1倍(P均＜0.05＝.免疫组织化学结果可见空白对照组及IPC组非缺血区心肌组织中脂联素未染色,而缺血的心肌组织局部脂联素染色加深,即脂联素在缺血区的表达明显高于非缺血区(P＜0.05＝.IPC组0、6和12 h亚组大鼠血浆中脂联素水平均显著高于空白对照组各相应时间点亚组(0 h:10.90±1.74比7.40±0.47;6 h:10.98±1.74比8.18±1.41;12 h:9.31±0.96比6.97±1.02,P均＜0.05＝.结论 IPC可减少心肌梗死的面积.IPC后心肌组织和血浆中脂联素表达水平均升高,提示脂联素参与了IPC的心肌保护作用.
목적 통과건립대서심기결혈예처리(IPC)모형급심기경사모형,탐토IPC대심기적보호작용급기대지련소표체적영향.방법 성년대서(4월령)건립IPC모형급IPC후심기경사모형,수궤분위공백대조조(0、6、12화24 h아조)、IPC조(0、6、12화24 h아조)、단순심기경사(MI)조급IPC+MI조.채용Masson삼색염색법측량심기경사면적(유두기평면경사심기여좌심실심기면적적비치,%),면역조직화학법화실시형광정량PCR법검측지련소재심기조직중적단백화mRNA표체수평,이용대서혈장표본주매련면역흡부실험,관찰순배중지련소함량적변화.결과 IPC+MI조대서심기경사면적명현소우MI조[(20±2)%비(31±3)%,P＜0.05＝.IPC조6화12 h아조대서심기조직중지련소mRNA적표체분별시공백대조조상응시간점아조적2.2배화2.1배(P균＜0.05＝.면역조직화학결과 가견공백대조조급IPC조비결혈구심기조직중지련소미염색,이결혈적심기조직국부지련소염색가심,즉지련소재결혈구적표체명현고우비결혈구(P＜0.05＝.IPC조0、6화12 h아조대서혈장중지련소수평균현저고우공백대조조각상응시간점아조(0 h:10.90±1.74비7.40±0.47;6 h:10.98±1.74비8.18±1.41;12 h:9.31±0.96비6.97±1.02,P균＜0.05＝.결론 IPC가감소심기경사적면적.IPC후심기조직화혈장중지련소표체수평균승고,제시지련소삼여료IPC적심기보호작용.
Objective To investigate whether adiponectin plays a role in the protection of myocardium in the rat myocardial ischemia preconditioning (IPC) model. Method Infarct size was measured by Masson's Trichrome staining, the expression of protein and mRNA of adiponectin at 0, 6, 12 and 24 h after IPC was examined by immunohistochemistry and quantitative real time RT-PCR, plasma levels of adiponectin at above mentioned four time points after IPC were detected by ELISA in IPC and MI rats. Result Infarct size was smaller in IPC than in MI rats (20% ±2% vs. 31% ±3%, P＜0. 05). The expression of adiponectin mRNA at 6 h and 12 h after IPC was 2. 2 and 2. 1 times higher than in Sham rats at respective time points (P ＜ 0. 05 ). Immunohistochemistry staining evidenced increased adiponectin expression in the ischemic area and weak expression of adiponectin in non-ischemic area ( P ＜ 0. 05 ).Compared to the sham group, the plasma level of adiponectin increased significantly at 0, 6 and 12 h after IPC (0 h:7.40 ±0.47 vs. 10.90 ±1.74;6 h: 8. 18 ±1.41 vs. 10.98 ±1.74;12 h:6. 97±1.02 vs. 9. 31 ±0. 96, P ＜ 0. 05 ). Conclusion IPC reduced infarction size, upregulated the myocardial expression of adiponectin at mRNA and protein levels, and increased plasma adiponectin concentration, suggesting that the adiponecitn may play a critical role in the protective effect of IPC.