Abstract
Background Chronic heart failure (CHF) is a serious heart disease resulting from cardiac dysfunction. Oxidative stress is an important factor in aging and disease. Butein, however, has antioxidant properties. To determine the effect of butein on oxidative stress injury in rats, a CHF rat model was established. Methods The CHF rat model was induced by abdominal aortic coarctation (AAC). Rats in CHF+butein and sham+butein group were given 100 mg/kg butein via gavage every day to detect the effect of butein on oxidative stress injury and myocardial dysfunction. The cardiac structural and functional parameters, including the left ventricular end-systolic dimension (LVESD), the left ventricular end-diastolic dimension (LVEDD), the left ventricular ejection fraction (LVEF), and the left ventricular fractional shortening (LVFS), were measured. Oxidative stress was measured through the production of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA). Cardiac injury markers like creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) were evaluated. Hematoxylin and eosin (H&E) staining was used to observe the myocardial cell morphology. The effect of butein on the extracellular signal-regulated kinase (ERK)/nuclear factor-E2 p45-related factor (Nrf2) signaling was confirmed by Western blot analysis. Results Butein had a significant effect on CHF in animal models. In detail, butein inhibited oxidative stress, relieved cardiac injury, and alleviated myocardial dysfunction. Importantly, butein activated the ERK1/2 pathway, which contributed to Nrf2 activation and subsequent heme oxygenase-1 (HO-1) and glutathione cysteine ligase regulatory subunit (GCLC) induction. Conclusions In this study, butein inhibits oxidative stress injury in CHF rat model via ERK/Nrf2 signaling pathway.
Highlights
As a common chronic cardiovascular disease, chronic heart failure (CHF) has a high mortality rate of incidence, which is up to 20% [1,2,3]
left ventricular end-systolic dimension (LVESD) and left ventricular end-diastolic dimension (LVEDD) doubled in Chronic heart failure (CHF)+phosphate buffer saline (PBS) group, compared with those in sham+PBS group, while butein partially reversed the increase in CHF+PBS group (Figures 1(a) and 1(b))
left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were reduced in CHF+PBS group, compared with those in sham+PBS group, while butein restored LVEF and LVFS to normal levels, suggesting the protective role of butein in CHF (Figures 1(c) and 1(d))
Summary
As a common chronic cardiovascular disease, chronic heart failure (CHF) has a high mortality rate of incidence, which is up to 20% [1,2,3]. The prevention and existing treatment strategies of oxidative stress in CHF are not effective in improving the survival rate, so further studies are urgently needed. Chronic heart failure (CHF) is a serious heart disease resulting from cardiac dysfunction. Oxidative stress is an important factor in aging and disease. To determine the effect of butein on oxidative stress injury in rats, a CHF rat model was established. Rats in CHF+butein and sham+butein group were given 100 mg/kg butein via gavage every day to detect the effect of butein on oxidative stress injury and myocardial dysfunction. Butein inhibited oxidative stress, relieved cardiac injury, and alleviated myocardial dysfunction. Butein inhibits oxidative stress injury in CHF rat model via ERK/ Nrf signaling pathway
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