FOLLOWUS
1. Institute of Cardiovascular Disease Research, Xuzhou Medical College,Jiangsu Province,Xuzhou,China
2. Department of Physiology, Xuzhou Medical College,Jiangsu Province,Xuzhou,China
纸质出版日期:2017,
网络出版日期:2016-3-8,
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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, 2017,23(7):518-527.
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, 2017,23(7):518-527. DOI: 10.1007/s11655-015-2296-x.
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.
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.
luteolincardiomyocyteischemia/reperfusioncardioprotection
luteolincardiomyocyteischemia/reperfusioncardioprotection
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