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Chin J Integr Med. 2017 Jul;23(7):518-527. doi: 10.1007/s11655-015-2296-x. Epub 2016 Mar 8.

Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart.

Author information

1
Institute of Cardiovascular Disease Research, Xuzhou Medical College, Xuzhou, Jiangsu Province, 221002, China.
2
Institute of Cardiovascular Disease Research, Xuzhou Medical College, Xuzhou, Jiangsu Province, 221002, China. dongyelichina@gmail.com.
3
Department of Physiology, Xuzhou Medical College, Xuzhou, Jiangsu Province, 221002, China. sunh@xzmc.edu.cn.

Abstract

OBJECTIVE:

To investigate the antioxidative effect and mechanism of luteolin on rat cardiomyocytes and isolated hearts followed by simulated ischemia/reperfusion (SI/R) injury.

METHODS:

The left ventricular cardiomyocytes and the isolated hearts from adult rats were subjected to SI/R injury. The experiment groups included control, SI/R, luteolin + SI/R (Lut + SI/R), vitamin E (Vit E) + SI/R, and LY294002 + luteolin + SI/R (LY + Lut + SI/R) groups. Cell viability, shortening amplitude, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity, the production of reactive oxygen species (ROS) and malondialdehyde (MDA), expression levels of Akt, phosphorylated Akt, NOX2 (gp91phox), NOX2 mRNA, mitogen-activated protein kinase (p38 MAPK) and phosphorylated p38MAPK were all measured after 3-h simulated ischemia and 2-h simulated reperfusion procedure in cardiomyocytes. Vit E was used as a standard control. The contractile function of isolated hearts was further observed after they were subjected to 30-min global ischemia and 120-min reperfusion.

RESULTS:

Pretreatment with 8-μmol/L luteolin substantially increased cell viability and shortening amplitude, while reducing evidence of oxidative stress-induced damage in the cells. In addition, the expression of NOX2, NOX2 mRNA and phosphorylation of p38MAPK were all downregulated. Furthermore, pretreatment with 40-μmol/L luteolin improved the recovery of myocardial contractile function following SI/R-induced injury, and luteolin markedly increased phosphorylation of Akt. However, all of the above effects were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002.

CONCLUSIONS:

Luteolin prevents SI/R-induced myocardial damage by reducing oxidative stress-induced injury in isolated rat hearts and cardiomyocytes, and the cardioprotection induced by luteolin was partially mediated by the PI3K/Akt pathway.

KEYWORDS:

cardiomyocyte; cardioprotection; ischemia/reperfusion; luteolin

PMID:
26956461
DOI:
10.1007/s11655-015-2296-x
[Indexed for MEDLINE]

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