内吗啡肽-1后处理的心肌保护作用及其对Erk1/2信号通路的影响
目的探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2（Erk1/2）信号转导通路的影响。方法构建在体大鼠心肌缺血再灌注模型,分假手术组、缺血再灌注组、内吗啡肽-1后处理组（EM50组）、PD98059后处理组（PD组）、内吗啡肽-1＋PD98059后处理组（EM50＋PD组）。实时记录各组大鼠血流动力学指标,采集复灌结束后大鼠血清,检测超氧化物歧化酶、丙二醛、白介素-6、肿瘤坏死因子-α乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白等心肌酶学及生化指标,大鼠心肌组织HE病理染色,TTC双染色法测定心肌梗死面积,Western-blot检测各组心肌组织中P-Erk1...
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| Published in | 南方医科大学学报 Vol. 37; no. 8; pp. 1028 - 1034 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | Chinese |
| Published |
蚌埠医学院科研中心,安徽 蚌埠 233030
2017
蚌埠医学院生理学教研室,安徽 蚌埠,233030%蚌埠医学院生理学教研室,安徽 蚌埠 233030 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1673-4254 |
| DOI | 10.3969/j.issn.1673-4254.2017.08.05 |
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| Abstract | 目的探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2（Erk1/2）信号转导通路的影响。方法构建在体大鼠心肌缺血再灌注模型,分假手术组、缺血再灌注组、内吗啡肽-1后处理组（EM50组）、PD98059后处理组（PD组）、内吗啡肽-1＋PD98059后处理组（EM50＋PD组）。实时记录各组大鼠血流动力学指标,采集复灌结束后大鼠血清,检测超氧化物歧化酶、丙二醛、白介素-6、肿瘤坏死因子-α乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白等心肌酶学及生化指标,大鼠心肌组织HE病理染色,TTC双染色法测定心肌梗死面积,Western-blot检测各组心肌组织中P-Erk1/2及凋亡相关蛋白Cleaved caspase-3的变化。结果与假手术组比较,缺血再灌注组心率和血压降低（P〈0.05）;与缺血再灌注组比较,EM50组心率和血压有所增高（P〈0.05）,血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量下降;超氧化物歧化酶活性增加（P〈0.05）;心肌梗死面积减少（P〈0.05）;P-Erk1/2表达增加（P〈0.05）;Cleaved Caspase-3表达降低（P〈0.05）。与EM50组比较,EM50＋PD组心率和血压降低（P〈0.05）,血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量增加,超氧化物歧化酶活性降低（P〈0.05）;心肌梗死面积增加（P〈0.05）;P-Erk1/2表达降低（P〈0.05）;Cleaved Caspase-3表达增加。结论内吗啡肽-1后处理可能通过改善心功能、抑制炎症反应、抑制氧化应激发挥保护作用;内吗啡肽-1改善大鼠心肌缺血再灌注损伤的过程中,存在Erk1/2信号通路的激活。 |
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| AbstractList | 目的探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2（Erk1/2）信号转导通路的影响。方法构建在体大鼠心肌缺血再灌注模型,分假手术组、缺血再灌注组、内吗啡肽-1后处理组（EM50组）、PD98059后处理组（PD组）、内吗啡肽-1＋PD98059后处理组（EM50＋PD组）。实时记录各组大鼠血流动力学指标,采集复灌结束后大鼠血清,检测超氧化物歧化酶、丙二醛、白介素-6、肿瘤坏死因子-α乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白等心肌酶学及生化指标,大鼠心肌组织HE病理染色,TTC双染色法测定心肌梗死面积,Western-blot检测各组心肌组织中P-Erk1/2及凋亡相关蛋白Cleaved caspase-3的变化。结果与假手术组比较,缺血再灌注组心率和血压降低（P〈0.05）;与缺血再灌注组比较,EM50组心率和血压有所增高（P〈0.05）,血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量下降;超氧化物歧化酶活性增加（P〈0.05）;心肌梗死面积减少（P〈0.05）;P-Erk1/2表达增加（P〈0.05）;Cleaved Caspase-3表达降低（P〈0.05）。与EM50组比较,EM50＋PD组心率和血压降低（P〈0.05）,血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量增加,超氧化物歧化酶活性降低（P〈0.05）;心肌梗死面积增加（P〈0.05）;P-Erk1/2表达降低（P〈0.05）;Cleaved Caspase-3表达增加。结论内吗啡肽-1后处理可能通过改善心功能、抑制炎症反应、抑制氧化应激发挥保护作用;内吗啡肽-1改善大鼠心肌缺血再灌注损伤的过程中,存在Erk1/2信号通路的激活。 目的 探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2(Erk1/2)信号转导通路的影响.方法 构建在体大鼠心肌缺血再灌注模型,分假手术组、缺血再灌注组、内吗啡肽-1后处理组(EM50组)、PD98059后处理组(PD组)、内吗啡肽-1+PD98059后处理组(EM50+PD组).实时记录各组大鼠血流动力学指标,采集复灌结束后大鼠血清,检测超氧化物歧化酶、丙二醛、白介素-6、肿瘤坏死因子-α乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白等心肌酶学及生化指标,大鼠心肌组织HE病理染色,TTC双染色法测定心肌梗死面积,Western-blot检测各组心肌组织中P-Erk1/2及凋亡相关蛋白Cleaved caspase-3的变化.结果 与假手术组比较,缺血再灌注组心率和血压降低(P<0.05);与缺血再灌注组比较,EM50组心率和血压有所增高(P<0.05),血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量下降;超氧化物歧化酶活性增加(P<0.05);心肌梗死面积减少(P<0.05);P-Erk1/2表达增加(P<0.05);Cleaved Caspase-3表达降低(P<0.05).与EM50组比较,EM50+PD组心率和血压降低(P<0.05),血浆中乳酸脱氢酶、肌酸激酶、心肌肌钙蛋白、丙二醛、白介素-6、肿瘤坏死因子-α活性或含量增加,超氧化物歧化酶活性降低(P<0.05);心肌梗死面积增加(P<0.05);P-Erk1/2表达降低(P<0.05);Cleaved Caspase-3表达增加.结论 内吗啡肽-1后处理可能通过改善心功能、抑制炎症反应、抑制氧化应激发挥保护作用;内吗啡肽-1改善大鼠心肌缺血再灌注损伤的过程中,存在Erk1/2信号通路的激活. |
| Abstract_FL | Objective To investigate the effect of postischemic treatment with endomorphin-1 (EM-1) against myocardial ischemia/reperfusion (IR) injury in rats and on extracellular signal regulated kinase 1/2 (Erk1/2)-dependent signaling pathway. Methods Sprague-Dawley rats were randomly divided into 5 groups, namely the sham-operated group, IR group, EM-1 post-treatment group (EM50 group), EM-1 post-treatment group with PD98059 treatment (EM50+PD group), and PD98059 post-treatment group (PD group). The hemodynamic indexes of the rats were recorded. After reperfusion, CK-MB, LDH, CTnI, MDA, IL-6, TNF-α, and SOD activities or contents were measured, the infarct size was determined, and the expression levels of Erk1/2, P-Erk1/2 and cleaved caspase-3 were detected using Western blotting. Results Compared with the sham group, the IR group showed significantly decreased heart rate and mean arterial pressure (P<0.05), which were increased obviously by EM-1 post-treatment (P<0.05). EM-1 post-treatment also resulted in significantly decreased LDH, CK-MB, CTnI, MDA, IL-6, and TNF-αactivities or contents (P<0.05), increased SOD activity (P<0.05), reduced the infarct size (P<0.05), and increased the expression level of P-Erk protein (P<0.05). Compared with EM50 group, EM50+PD group showed significantly decreased heart rate and mean arterial pressure (P<0.05), increased LDH, CK-MB, CTnI, MDA, IL-6, and TNF-αactivities or contents (P<0.05), decreased SOD activity, increased infarct size (P<0.05), and lowered expression of P-Erk protein (P<0.05). Conclusion Postischemic treatment with EM-1 protects the heart against IR injury by improving the cardiac function, inhibiting inflammation, and inhibiting oxidative stress and myocardial apoptosis, and Erk1/2 signaling pathway may be involved in this process. |
| Author | 王娅 刘明珠 李红俊 张蔚屏 高琴 李正红 |
| AuthorAffiliation | 蚌埠医学院生理学教研室,安徽蚌埠233030 蚌埠医学院生理学教研室,安徽蚌埠233030;蚌埠医学院科研中心,安徽蚌埠233030 |
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| Author_FL | WANG Ya LIU Mingzhu ZHANG Weiping GAO Qin LI Hongjun LI Zhenghong |
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| Keywords | 细胞外信号调节激酶1/2 心肌缺血后处理 心肌保护 endomorphin-1 ischemia postconditioning cardioprotection 内吗啡肽 |
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| Notes | 44-1627/R ischemia postconditioning;cardioprotection Objective To investigate the effect of postischemic treatment with endomorphin-1 （EM-1） against myocardial ischemia/reperfusion （IR） injury in rats and on extracellular signal regulated kinase 1/2 （Erk1/2）-dependent signaling pathway. Methods Sprague-Dawley rats were randomly divided into 5 groups, namely the sham-operated group, IR group, EM-1 post-treatment group （EM50 group）, EM-1 post-treatment group with PD98059 treatment （EM50＋PD group）, and PD98059 post-treatment group （PD group）. The hemodynamic indexes of the rats were recorded. After reperfusion, CK-MB, LDH, CTnI, MDA, IL-6, TNF-α, and SOD activities or contents were measured, the infarct size was determined, and the expression levels of Erk1/2, P-Erk1/2 and cleaved caspase-3 were detected using Western blotting. Results Compared with the sham group, the IR group showed significantly decreased heart rate and mean arterial pressure （P〈0.05）, which were increased obviously by EM-1 post-treatment （P〈0. |
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| Publisher | 蚌埠医学院科研中心,安徽 蚌埠 233030 蚌埠医学院生理学教研室,安徽 蚌埠,233030%蚌埠医学院生理学教研室,安徽 蚌埠 233030 |
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| Snippet | 目的探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2（Erk1/2）信号转导通路的影响。方法构建在体大鼠心肌缺血再灌注模型,分假手... 目的 探讨在大鼠心肌缺血再灌注过程中,内吗啡肽-1后处理的心肌保护作用对细胞外信号调节激酶1/2(Erk1/2)信号转导通路的影响.方法 构建在体大鼠心肌缺血再灌注模型,分假手... |
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| SubjectTerms | 内吗啡肽 心肌保护 心肌缺血后处理 细胞外信号调节激酶1/2 |
| Title | 内吗啡肽-1后处理的心肌保护作用及其对Erk1/2信号通路的影响 |
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