Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury
文献类型：期刊论文
| 作者 | Yu, Dongsheng ; Li, Mengwen ; Tian, Youqing ; Liu, Jun ; Shang, Jing ; Shang, J (reprint author), China Pharmaceut Univ, Ctr Drug Screening, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China. |
| 刊名 | LIFE SCIENCES
 |
| 出版日期 | 2015-02-01 |
| 英文摘要 | Aims: Luteolin is a falconoid compound that has an antioxidant effect, but its contribution to ROS-activated MAPK pathways in ischemia/reperfusion injury is seldom reported. Here, we have confirmed that it exhibits an antioxidant effect in myocardial ischemia/reperfusion injury (MIRI) by inhibiting ROS-activated MAPK pathways. Main methods: We exposed rat hearts into the left anterior descending coronary artery (LAD) ligation for 30 min followed by 1 h of reperfusion. Observations were carried out using electrocardiography; detection of hemodynamic parameters; and testing levels of lactate dehydrogenase (LDH), creatine kinase (CK), total superoxide dismutase (T-SOD), and malondialdehyde (MDA). Mitogen-activated protein kinase (MAPK) pathway was measured by western blot and transmission electron microscopy was applied to observe the myocardial ultrastructure. Rat H9c2 cell in 95% N-2 and 5% CO2 stimulated the MIRI. Oxidation system mRNA levels were measured by real-time PCR; mitochondrial membrane potential and apoptosis were measured by confocal microscopy and flow cytometry; western blot analysis was used to assay caspase-3, -8, and -9 and MAPK pathway protein expression; the MAPK pathway was inhibited using SB203580 (p38 MAPK inhibitor) and SP600125 (c-Jun NH2-terminal kinase inhibitor) before H9c2 cells were exposed to hypoxia/reoxygenation injury to show the modulation of the changes in ROS generation, cell viability and apoptosis. Key findings: In vivo, luteolin can ameliorate the impaired mitochondrial morphology, regulating the MAPK pathway to protect MIRI. In vitro, luteolin can affect the oxidation system, mitochondrial membrane potential and MAPK pathway to anti-apoptosis. Significance: These results reveal a ROS-MAPK mediated mechanism and mitochondrial pathway through which luteolin can protect myocardial ischemia/reperfusion injury. (C) 2014 Elsevier Inc. All rights reserved.; Aims: Luteolin is a falconoid compound that has an antioxidant effect, but its contribution to ROS-activated MAPK pathways in ischemia/reperfusion injury is seldom reported. Here, we have confirmed that it exhibits an antioxidant effect in myocardial ischemia/reperfusion injury (MIRI) by inhibiting ROS-activated MAPK pathways. |
| 源URL | [http://210.75.249.4/handle/363003/5458]  |
| 专题 | 西北高原生物研究所_中国科学院西北高原生物研究所 |
| 推荐引用方式 GB/T 7714 | Yu, Dongsheng,Li, Mengwen,Tian, Youqing,et al. Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury[J]. LIFE SCIENCES,2015. |
| APA | Yu, Dongsheng,Li, Mengwen,Tian, Youqing,Liu, Jun,Shang, Jing,&Shang, J .(2015).Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury.LIFE SCIENCES. |
| MLA | Yu, Dongsheng,et al."Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury".LIFE SCIENCES (2015). |
入库方式： OAI收割
来源：西北高原生物研究所
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