Liraglutide is glucagon-like peptide-1 receptor agonist used for treating patients with type 2 diabetes mellitus. The present study aimed to investigate the role and mechanism of liraglutide in repairing the infarcted heart following myocardial infarction. The results of the present study demonstrated that amplification of the dose of liraglutide for ~28 days was able to reduce cardiac fibrosis, inflammatory responses and myocardial death in the post-infarcted heart. In vitro, liraglutide protected cardiomyocyte mitochondria against the chronic hypoxic damage, inhibiting the mitochondrial apoptosis pathways. Mechanistically, liraglutide elevated the expression of NAD-dependent protein deacetylase sirtuin-1 (SIRT1), which increased the expression of Parkin, leading to mitophagy activation. Protective mitophagy reversed cellular adenosine 5′-triphosphate production, reduced cellular oxidative stress and balanced the redox response, sustaining mitochondrial homeostasis. Notably, following blockade of glucagon-like peptide 1 receptor or knockdown of Parkin, the beneficial effects of liraglutide on mitochondria disappeared. In conclusion, the results of the present study illustrated the protective role of liraglutide in repairing the infarcted heart via regulation of the SIRT1/Parkin/mitophagy pathway.
This study aims to investigate the changes of aquaporin-4 (AQP4), β-amyloid precursor proteins (APP) and β-amyloid (Aβ) in brain tissues after cerebral ischemiareperfusion injury (CIRI), and evaluate the effect of edaravone. The Middle Cerebral Artery Occlusion was used to establish CIRI in rats. Rats were divided into control, model and edaravone groups. The neurological deficits in the model group were obvious and the neurological score increased compared to the control group, while the neurological deficits of the edaravone group were improved as the neurological score decreased compared to the model group. The number of pyramidel cells in the hippocampus of the model group was significantly decreased whereas edaravone could reverse this decrease. The model group had significantly higher levels of Aβ, APP and AQP4 than the control group and edaravone group, suggesting that they might be involved in the neuronal cell damage. Meanwhile, the increased AQP4 might enhance the permeability of cells, and thus cause cell damage and neurological deficit. Conclusively, edaravone could reduce brain edema, protect neuronal cells and improve the neurological impairment of rats possibly by decreasing the expression of Aβ, APP and AQP4. Therefore, edaravone may have the potential to treat neurodegenerative diseases (such as Alzheimer's disease).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.