Hydrogen Attenuates Myocardial Injury in Rats by Regulating Oxidative Stress and NLRP3 Inflammasome Mediated Pyroptosis

Abstract

Purpose: Hydrogen (H2) is an antioxidant with anti-inflammatory and apoptosis functions.This study aimed to estimate the effects of H2 on acute myocardial infarction (AMI) in rats and its association with the inhibition of oxidative stress and cardiomyocyte pyroptosis. Methods: Sixty-four rats were randomly divided into three groups (Sham, AMI, and H2). The left anterior descending coronary artery (LAD) of rats in the AMI and H2 groups was ligated, while rats in the Sham group were threaded without ligation. In addition, 2% H2 was administered by inhalation for 24 h after ligation in the H2 group. Transthoracic echocardiography was performed after H2 inhalation, followed by collection of the serum and cardiac tissue of all rats. Results: H2 inhalation ameliorated the cardiac dysfunction, infarct size and inflammatory cell infiltration caused by AMI. Meanwhile, H2 inhalation reduced the concentration of serum Troponin I (TnI), brain natriuretic peptide (BNP), reactive oxygen species (ROS), cardiac malondialdehyde (MDA), and 8-OHdG. In addition, H2 inhalation inhibited cardiac inflammation and pyroptosis relative proteins expression. Conclusion: H2 effectively promoted heart functions in AMI rats by regulating oxidative stress and pyroptosis.

Study details

Article type

Original Research

Disease / injury model

Acute Myocardial Infarction (AMI)

Duration

24 hours

Dose-dependent effect

No

Outcome

Positive

Findings

Hydrogen inhalation (2% for 24h) significantly ameliorated cardiac dysfunction, reduced infarct size, decreased inflammatory cell infiltration, and lowered serum markers of cardiac injury and oxidative stress in a rat model of acute myocardial infarction. It also inhibited NLRP3 inflammasome activation and pyroptosis-related protein expression, suggesting a protective effect via regulation of oxidative stress and pyroptosis.