Effect of erythropoietin on expression of myocardial NADPH oxidase in pressure overload rats
10.3969/j.issn.1000-4718.2014.10.006
- VernacularTitle:促红细胞生成素对压力超负荷大鼠心肌NADPH 氧化酶表达的影响
- Author:
Liping WANG
;
Yu FAN
;
Man HAN
- Publication Type:Journal Article
- Keywords:
Erythropoietin;
Pressure overload;
NADPH oxidase
- From:
Chinese Journal of Pathophysiology
2014;(10):1760-1764
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the effect of erythropoietin ( EPO) on the expression of myocardial NADPH oxi-dase (Nox) in the pressure overload rats.METHODS:Male SD rats (n=36) were used to establish a pressure overload myocardial hypertrophy model by abdominal aorta ligation.The animals were divided into model group, control group ( sham, without narrowing abdominal aorta, the rest of the operation was the same as the model) and recombinant human erythropoietin ( rhEPO) treatment group ( intraperitoneal injection of rhEPO postoperatively, 4 000 U/kg, twice a week) . After 8 weeks, the cardiac ultrasound imaging and hemodynamic evaluation were conducted to determine the cardiac func-tions.Masson staining was used to observe the degree of myocardial fibrosis.The expression of Nox2 and Nox4 at mRNA and protein levels was detected by real-time quantitative PCR and Western blotting.The protein levels of myocardial inflam-matory factors CD45, F4/80 and TGF-βwere determined by Western blotting.RESULTS:Compared with model group, the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic pressure (LVESP) and left ventricular pressure maximum rising and falling rates ( ±dp/dtmax) increased significantly in EPO treatment group (P<0.01).At the same time, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter ( LVEDD) and left ventricular end-diastolic pressure ( LVEDP) were decreased in EPO treatment group (P<0.01).EPO reduced the degree of myocardial fibrosis caused by pressure overload (P<0.01) and decreased the ex-pression of Nox2 and Nox4 at mRNA and protein levels in the myocardium (P<0.05 or P<0.01), and reduced the pro-tein expression of myocardial inflammatory factors CD45, F4/80 and TGF-β.CONCLUSION: EPO inhibits rat myocar-dial fibrosis induced by pressure overload, improves heart functions by decreasing NADPH oxidase activity and inhibiting myocardial oxidative stress levels and myocardial inflammatory reaction.
