Protective effects of Apelin-13 on nicotine-induced H9c2 cardiomyocyte apoptosis and oxidative stress.

ABSTRACT:

Introduction

We aimed to explore the role of Apelin-13 in resisting oxidation, inflammation as well as apoptosis and its underlying mechanisms of action using a model of nicotine-induced H9c2 cardiomyocyte injury.

Methods

H9c2 cardiomyocytes were randomly divided into control, nicotine, nicotine + Apelin-13, and Apelin-13 groups. Cell counting kit-8 assay was conducted to determine the cell viability. Interleukin (IL)-6, superoxide dismutase, tumor necrosis factor-alpha (TNF-α), glutathione peroxidase (GSH-Px), IL-β, catalase (CAT), IL-8, lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels were examined. A 2',7'-dichlorodihydrofluorescein diacetate assay was conducted to measure the intracellular reactive oxygen species (ROS) level. The morphology of apoptotic card

SUBMITTER: Xu C 

PROVIDER: S-EPMC11915093 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature