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

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.

Butein Ameliorates Oxidative Stress in H9c2 Cardiomyoblasts through Activation of the NRF2 Signaling Pathway

“…Many previous studies have been reported that butein is involved in the development of a variety of chronic diseases, such as cancers [ 27 , 28 ], nephritis [ 29 ], obesity [ 30 ], diabetes [ 31 ], and hypertension [ 32 ]. In particular, a recent study demonstrated that butein protected heart function from oxidative injury through the extracellular signal-regulated kinase (ERK)/Nrf2 signaling pathway in a chronic heart failure rat model [ 33 ]. However, an in-depth study focusing on oxidative stress itself has not been conducted.…”

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“…[18]. Currently, studies have confirmed that the transduction of ERK signaling pathway is closely linked to both inflammatory response and oxidative stress [19]. Meanwhile, Li YH et al also showed that botulinum toxin type A decreased the proliferation of fibroblasts and prevented overdeposition of ECM through the inhibition of the TGF-β1/Smad and ERK pathways [20].…”

Mechanisms of action of natural small-molecule drugs in cardiovascular disease

“…In vivo , pyruvate kinase isozyme type M2 (PKM2) inhibition by shikonin attenuated Ang-II-induced cardiomyocyte hypertrophy and fibrosis by inhibiting the cardiac remodeling pathway and oxidative stress by inhibiting TGF-β/Smad2/3 and Jak2/Stat3 signaling [108]. Butein inhibited oxidative stress injury-induced ERK/Nrf2 signaling [109].…”