Protective effects of Apelin-13 on nicotine-induced H9c2 cardiomyocyte apoptosis and oxidative stress
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 +...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2025-03-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | https://www.tobaccoinduceddiseases.org/Protective-effects-of-Apelin-13-on-nicotine-induced-H9c2-cardiomyocyte-apoptosis,201400,0,2.html |
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| Summary: | 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 cardiomyocytes was observed by 4',6-diamidino-2-phenylindole
staining. Western blotting was employed to measure the protein expressions
of apoptotic factors B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax).
Apoptosis was quantified using Annexin V/propidium iodide staining.
Results
Exposure of H9c2 cardiomyocytes to 10 μM nicotine significantly reduced
cell viability and increased LDH release, oxidative stress (elevated MDA and
ROS levels with decreased superoxide dismutase, GSH-Px, and CAT activities),
pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-8), and apoptotic markers
(increased Bax with decreased Bcl-2 expression, along with nuclear condensation)
(p<0.05). In contrast, treatment with 2 μM Apelin-13 significantly alleviated
these deleterious effects, enhancing cell viability, restoring antioxidant enzyme
activities, reducing oxidative and inflammatory responses, and inhibiting apoptosis
(p<0.05).
Conclusions
Nicotine induction increases the oxidative stress and apoptotic capacity
of H9c2 cardiomyocytes, but Apelin-13 protects H9c2 cardiomyocytes against
nicotine-induced apoptosis and oxidative stress. |
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| ISSN: | 1617-9625 |