Background: Atrial fibrillation (AF) is often associated with atrial fibrosis and oxidative stress. Neferine, a bisbenzylisoquinoline alkaloid, has been reported to exert an antiarrhythmic effect. However, its impact on Angiotensin II (Ang II) infusion-induced AF and the underlying mechanism remains unclear. This study aimed to investigate whether neferine alleviates Ang II-induced AF and explore the underlying mechanisms.
Methods: Mice subjected to Ang II infusion to induce AF were concurrently treated with neferine or saline. AF incidence, myocardial cell size, fibrosis, and oxidative stress were then examined.
Results: Neferine treatment inhibited Ang II-induced AF, atrial size augmentation, and atrial fibrosis. Additionally, we observed that Ang II increased reactive oxygen species (ROS) generation, induced mitochondrial membrane potential depolarization, and reduced glutathione (GSH) and superoxide dismutase (SOD) levels, which were reversed to some extent by neferine. Mechanistically, neferine activated the Nrf2/HO-1 signaling pathway and inhibited TGF-β/p-Smad2/3 in Ang II-infused atria. Zinc Protoporphyrin (ZnPP), an HO-1 inhibitor, reduced the anti-oxidative effect of neferine to some extent and subsequently abolished the beneficial effect of neferine on Ang II-induced AF.
Conclusions: These findings provide hitherto undocumented evidence that the protective role of neferine in Ang II-induced AF is dependent on HO-1.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11164477 | PMC |
http://dx.doi.org/10.18632/aging.205829 | DOI Listing |
ACS Appl Bio Mater
December 2024
Department of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P. R. China.
Abdominal aortic aneurysm (AAA) is a cardiovascular disease with potentially fatal consequences, yet effective therapies to prevent its progression remain unavailable. Oxidative stress is associated with AAA development. Carbon dots have reactive oxygen species-scavenging activity, while green tea extract exhibits robust antioxidant properties.
View Article and Find Full Text PDFClin Transl Med
January 2025
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Sporadic aortic aneurysm and dissection (AAD) is a critical condition characterised by the progressive loss of vascular smooth muscle cells (VSMCs) and the breakdown of the extracellular matrix. However, the molecular mechanisms responsible for the phenotypic switch and loss of VSMCs in AAD are not fully understood.
Methods And Results: In this study, we employed a discovery-driven, unbiased approach.
Redox Biol
December 2024
Department of Biochemistry and Molecular Biology, School of Basic Medicine, Guizhou Medical University, Gui'an, 561113, Guizhou, PR China. Electronic address:
NADPH oxidase 1 (Nox1) is a major isoform of Nox in vascular smooth muscle cells (VSMCs). VSMC activation and extracellular matrix (ECM) remodelling induce abdominal aortic aneurysm (AAA). In this study, we aim to determine the role of Nox1 in the progression of AAA and explore the underling mechanism.
View Article and Find Full Text PDFAdv Healthc Mater
December 2024
Department of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325027, P. R. China.
The abdominal aortic aneurysm (AAA) is a severe and complex condition characterized by the pathological dilation of the abdominal aorta. Current therapeutic strategies are limited, with surgical repair being the most effective intervention due to the lack of medications that can slow aneurysmal expansion or prevent adverse events. In this study, an innovative nanoplatform, Mn-UiO-66-NH@HA, designed to repair vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM) is developed, thereby enhancing arterial wall integrity.
View Article and Find Full Text PDFHypertens Res
December 2024
Department of Cardiology, Yijishan Hospital of Wannan Medical College, No. 2, Zheshan West Road, Wuhu, 241000, China.
Cardiac remodeling encompasses structural alterations such as hypertrophy, fibrosis, and dilatation, alongside numerous cellular and molecular functional aberrations, constituting a pivotal process in the advancement of heart failure (HF). 4-Hydroxychalcone (4-HCH) is a class of naturally occurring compounds with variable phenolic structures, and has demonstrated the preventive efficacy in hyperaldosteronism, inflammation and renal injury. However, the role of 4-HCH in the regulation of cardiac remodeling remains uncertain.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!