Alshehri Abdullah A, Al-Kuraishy Hayder M, Al-Gareeb Ali I, Jawad Sabrean F, Khawagi Wael Y, Alexiou Athanasios, Papadakis Marios, Assiri Abdullah A, Elhadad Heba, El-Saber Batiha Gaber
Department of Clinical Pharmacy, College of Pharmacy, Taif University, Al Huwaya, Taif, Saudi Arabia.
Department of Clinical Pharmacology and Medicine, College of Medicine, Al-Mustansiriya University, Baghdad, Iraq.
J Inflamm (Lond). 2024 Jun 10;21(1):19. doi: 10.1186/s12950-024-00394-x.
Atherosclerosis (AS) formation is enhanced by different mechanisms including cytokine generation, vascular smooth muscle cell proliferation, and migration. One of the recent treatments towards endothelial dysfunction and AS is Vinpocetine (VPN). VPN is a potent inhibitor of phosphodiesterase enzyme 1 (PDE-1) and has anti-inflammatory and antioxidant effects through inhibition the expression of nuclear factor kappa B (NF-κB). VPN has been shown to be effective against the development and progression of AS. However, the underlying molecular mechanism was not fully clarified. Consequently, objective of the present review was to discuss the mechanistic role of VPN in the pathogenesis AS. Most of pro-inflammatory cytokines that released from macrophages are inhibited by action of VPN through NF-κB-dependent mechanism. VPN blocks monocyte adhesion and migration by constraining the expression and action of pro-inflammatory cytokines. As well, VPN is effective in reducing of oxidative stress a cornerstone in the pathogenesis of AS through inhibition of NF-κB and PDE1. VPN promotes plaque stability and prevents the erosion and rupture of atherosclerotic plaque. In conclusion, VPN through mitigation of inflammatory and oxidative stress, and improvement of plaque stability effects could be effective agent in the management of AS.
动脉粥样硬化（AS）的形成通过多种机制增强，包括细胞因子生成、血管平滑肌细胞增殖和迁移。长春西汀（VPN）是近年来针对内皮功能障碍和AS的一种治疗方法。VPN是磷酸二酯酶1（PDE-1）的有效抑制剂，通过抑制核因子κB（NF-κB）的表达具有抗炎和抗氧化作用。已证明VPN对AS的发展和进展有效。然而，其潜在的分子机制尚未完全阐明。因此，本综述的目的是探讨VPN在AS发病机制中的作用机制。巨噬细胞释放的大多数促炎细胞因子通过VPN的作用通过NF-κB依赖性机制受到抑制。VPN通过抑制促炎细胞因子的表达和作用来阻止单核细胞的粘附和迁移。此外，VPN通过抑制NF-κB和PDE1有效降低氧化应激，氧化应激是AS发病机制的一个基石。VPN促进斑块稳定性，防止动脉粥样硬化斑块的侵蚀和破裂。总之，VPN通过减轻炎症和氧化应激以及改善斑块稳定性效应，可能是AS管理中的有效药物。
