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Atheroprotective role of vinpocetine: an old drug with new indication

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Titel: Atheroprotective role of vinpocetine: an old drug with new indication
Autoren: Mohammed H. Abu-Alghayth, Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Athanasios Alexiou, Marios Papadakis, Mostafa M. Bahaa, Mohammed Afifi, Ammar AL-Farga, Eman Wahsh, Gaber El-Saber Batiha
Quelle: Inflammopharmacology
Verlagsinformationen: Springer Science and Business Media LLC, 2024.
Publikationsjahr: 2024
Schlagwörter: 0301 basic medicine, 0303 health sciences, NF-kappa B, Anti-Inflammatory Agents, Review, Atherosclerosis, Antioxidants, 3. Good health, Oxidative Stress, 03 medical and health sciences, Humans, Animals, Cytokines, Endothelium, Vascular, Antioxidants/pharmacology [MeSH], Endothelial dysfunction, Atherosclerosis/prevention, Humans [MeSH], Cytokines/metabolism [MeSH], Animals [MeSH], Endothelium, Vascular/drug effects [MeSH], Reactive oxygen species, Anti-Inflammatory Agents/pharmacology [MeSH], NF-kappa B/metabolism [MeSH], Vinpocetine, Atherosclerosis/drug therapy [MeSH], Oxidative Stress/drug effects [MeSH], Endothelium, Vascular/metabolism [MeSH], Vinca Alkaloids/pharmacology [MeSH], Atherosclerosis/metabolism [MeSH], Pro-inflammatory cytokines, Vinca Alkaloids
Beschreibung: Endothelial dysfunction is considered one of the main causes of atherosclerosis and elevated blood pressure. Atherosclerosis (AS) formation is enhanced by different mechanisms including cytokine generation, vascular smooth muscle cell proliferation, and migration. One of the recent treatment toward endothelial dysfunction is vinpocetine (VPN). VPN is an ethyl apovincaminate used in the management of different cerebrovascular disorders and endothelial dysfunction through inhibition of atherosclerosis formation. VPN is a potent inhibitor of phosphodiesterase enzyme 1 (PDE1) as well it has anti-inflammatory and antioxidant effects through inhibition of the expression of nuclear factor kappa B (NF-κB). VPN has been shown to be effective against development and progression of AS. However, the underlying molecular mechanism was not fully clarified. Consequently, objective of the present narrative review was to clarify the mechanistic role of VPN in AS. Most of pro-inflammatory cytokines released from macrophages are inhibited by the action of VPN via NF-κB-dependent mechanism. VPN blocks monocyte adhesion and migration by inhibiting the expression of pro-inflammatory cytokines. As well, VPN is effective in reducing oxidative stress, a cornerstone in the pathogenesis of AS, through inhibition of NF-κB and PDE1. VPN promotes plaque stability and prevent erosion and rupture of atherosclerotic plaque. In conclusion, VPN through mitigation of inflammatory and oxidative stress with plaque stability effects could be effective agent in the management of endothelial dysfunction through inhibition of atherosclerosis mediators.
Publikationsart: Article
Other literature type
Sprache: English
ISSN: 1568-5608
0925-4692
DOI: 10.1007/s10787-024-01529-5
Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/39141151
https://repository.publisso.de/resource/frl:6495866
Rights: CC BY
Dokumentencode: edsair.doi.dedup.....b65f247b10daa4b4a8bddc097689a821
Datenbank: OpenAIRE
Beschreibung
Abstract:Endothelial dysfunction is considered one of the main causes of atherosclerosis and elevated blood pressure. Atherosclerosis (AS) formation is enhanced by different mechanisms including cytokine generation, vascular smooth muscle cell proliferation, and migration. One of the recent treatment toward endothelial dysfunction is vinpocetine (VPN). VPN is an ethyl apovincaminate used in the management of different cerebrovascular disorders and endothelial dysfunction through inhibition of atherosclerosis formation. VPN is a potent inhibitor of phosphodiesterase enzyme 1 (PDE1) as well it has anti-inflammatory and antioxidant effects through inhibition of the expression of nuclear factor kappa B (NF-κB). VPN has been shown to be effective against development and progression of AS. However, the underlying molecular mechanism was not fully clarified. Consequently, objective of the present narrative review was to clarify the mechanistic role of VPN in AS. Most of pro-inflammatory cytokines released from macrophages are inhibited by the action of VPN via NF-κB-dependent mechanism. VPN blocks monocyte adhesion and migration by inhibiting the expression of pro-inflammatory cytokines. As well, VPN is effective in reducing oxidative stress, a cornerstone in the pathogenesis of AS, through inhibition of NF-κB and PDE1. VPN promotes plaque stability and prevent erosion and rupture of atherosclerotic plaque. In conclusion, VPN through mitigation of inflammatory and oxidative stress with plaque stability effects could be effective agent in the management of endothelial dysfunction through inhibition of atherosclerosis mediators.
ISSN:15685608
09254692
DOI:10.1007/s10787-024-01529-5