Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury

NWIPB OpenIR

	Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury
	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.
	2015-02-01
发表期刊	LIFE SCIENCES
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.
文献类型	期刊论文
条目标识符	http://210.75.249.4/handle/363003/32528
专题	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).