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

Rui-qu Zhang; Dong-ye Li; Tong-da Xu; Sha-sha Zhu; Huan-jun Pan; Fang Fang; Xin Wu; Hong Sun

doi:10.1007/s11655-015-2296-x

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

Updated：2021-08-27

- Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart
- Chinese Journal of Integrative Medicine Vol. 23, Issue 7, Pages: 518-527(2017)
- Affiliations：
  
  1. Institute of Cardiovascular Disease Research, Xuzhou Medical College,Jiangsu Province,Xuzhou,China
  2. Department of Physiology, Xuzhou Medical College,Jiangsu Province,Xuzhou,China
- Author bio：
- Funds：
  
  Supported by the Academic Degrees Committee and the Department of Education of Jiangsu Province (No. CXLX11-0732)
- DOI：10.1007/s11655-015-2296-x
  CLC：
- Published：2017，
  
  Published Online：8 March 2016，
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Zhang, Rq., Li, Dy., Xu, Td. et al. Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart., Chin. J. Integr. Med. 23, 518–527 (2017). https://doi.org/10.1007/s11655-015-2296-x

Rui-qu Zhang, Dong-ye Li, Tong-da Xu, et al. Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart. [J]. Chinese Journal of Integrative Medicine 23(7):518-527(2017)
Zhang, Rq., Li, Dy., Xu, Td. et al. Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart., Chin. J. Integr. Med. 23, 518–527 (2017). https://doi.org/10.1007/s11655-015-2296-x DOI：

Rui-qu Zhang, Dong-ye Li, Tong-da Xu, et al. Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart. [J]. Chinese Journal of Integrative Medicine 23(7):518-527(2017) DOI： 10.1007/s11655-015-2296-x.

摘要

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

Abstract

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

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. 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.

关键词

luteolincardiomyocyteischemia/reperfusioncardioprotection

Keywords

luteolincardiomyocyteischemia/reperfusioncardioprotection

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