Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway

Xin-Ji-Er-Kang (XJEK) inhibited cardiovascular remodeling in hypertensive mice in our previous studies. We hypothesized that XJEK may prevent isoproterenol (ISO)-induced myocardial hypertrophy (MH) in mice by ameliorating oxidative stress (OS) through a mechanism that may be related to the nuclear f...

Full description

Saved in:
Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2022-08, Vol.2022, p.1-11
Main Authors: Yu, Ting-Ting, Sun, Li-Jun, Chen, Chen, Wang, Zi-Jian, Liu, Xue-Sheng, Zhu, Feng-Qin, Gao, Shan
Format: Article
Language:English
Subjects:
Adrenergic receptors
Antioxidants
Atrial natriuretic peptide
Bioengineering
Brain natriuretic peptide
Catalase
Collagen
Echocardiography
EKG
Electrocardiography
Heart failure
Heme
Heme oxygenase (decyclizing)
Hypertension
Hypertrophy
Isoproterenol
Laboratory animals
Medical research
Metoprolol
Myosin
Nuclear transport
Oxidative stress
Oxygenase
Physiology
Proteins
Protocol
Signal transduction
Superoxide dismutase
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Xin-Ji-Er-Kang (XJEK) inhibited cardiovascular remodeling in hypertensive mice in our previous studies. We hypothesized that XJEK may prevent isoproterenol (ISO)-induced myocardial hypertrophy (MH) in mice by ameliorating oxidative stress (OS) through a mechanism that may be related to the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1(HO-1) pathways. Forty SPF male Kunming mice were randomized into 5 groups (n = 8 mice per group): control group, MH group, MH + different doses of XJEK (7.5 g/kg/day and 10 g/kg/day), and MH + metoprolol (60 mg/kg/day). On the eighth day after drug treatment, electrocardiogram (ECG) and echocardiography were performed, the mice were sacrificed, and blood and heart tissues were collected for further analysis. XJEK administration markedly ameliorated cardiovascular remodeling (CR), as manifested by a decreased HW/BW ratio and CSA and less collagen deposition after MH. XJEK administration also improved MH, as evidenced by decreased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-myosin heavy chain (β-MHC) levels. XJEK also suppressed the decreased superoxide dismutase (SOD) and catalase (CAT) activities and increased malondialdehyde (MDA) levels in serum of mice with MH. XJEK-induced oxidative stress may be related to potentiating Nrf2 nuclear translocation and HO-1 expression compared with the MH groups. XJEK ameliorates MH by activating the Nrf2/HO-1 signaling pathway, suggesting that XJEK is a potential treatment for MH.
ISSN:1741-427X
1741-4288
DOI:10.1155/2022/7229080