Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

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...

Full description

Saved in:
Bibliographic Details
Main Authors: Peng Liu (Author), Quanli Pan (Author)
Format: Book
Published: Hindawi-Wiley, 2022-01-01T00:00:00Z.
Subjects:
Online Access:Connect to this object online.
Tags: Add Tag
No Tags, Be the first to tag this record!

MARC

LEADER 00000 am a22000003u 4500
001 doaj_7f59b58ef12141e7adc300a7cd64d70d
042 |a dc 
100 1 0 |a Peng Liu  |e author 
700 1 0 |a Quanli Pan  |e author 
245 0 0 |a Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling 
260 |b Hindawi-Wiley,   |c 2022-01-01T00:00:00Z. 
500 |a 1755-5922 
500 |a 10.1155/2022/8684014 
520 |a 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. 
546 |a EN 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
690 |a Diseases of the circulatory (Cardiovascular) system 
690 |a RC666-701 
655 7 |a article  |2 local 
786 0 |n Cardiovascular Therapeutics, Vol 2022 (2022) 
787 0 |n http://dx.doi.org/10.1155/2022/8684014 
787 0 |n https://doaj.org/toc/1755-5922 
856 4 1 |u https://doaj.org/article/7f59b58ef12141e7adc300a7cd64d70d  |z Connect to this object online.