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Review
. 2014 Dec 26;20(1):335-47.
doi: 10.3390/molecules20010335.

Anti-inflammatory effects of vinpocetine in atherosclerosis and ischemic stroke: a review of the literature

Linjie Zhang  1 , Li Yang  2
Affiliations
Review

Anti-inflammatory effects of vinpocetine in atherosclerosis and ischemic stroke: a review of the literature

Linjie Zhang et al. Molecules. .

Abstract

Immune responses play an important role in the pathophysiology of atherosclerosis and ischemic stroke. Atherosclerosis is a common condition that increases the risk of stroke. Hyperlipidemia damages endothelial cells, thus initiating chemokine pathways and the release of inflammatory cytokines-this represents the first step in the inflammatory response to atherosclerosis. Blocking blood flow in the brain leads to ischemic stroke, and deprives neurons of oxygen and energy. Damaged neurons release danger-associated molecular patterns, which promote the activation of innate immune cells and the release of inflammatory cytokines. The nuclear factor κ-light-chain-enhancer of activated B cells κB (NF-κB) pathway plays a key role in the pathogenesis of atherosclerosis and ischemic stroke. Vinpocetine is believed to be a potent anti-inflammatory agent and has been used to treat cerebrovascular disorders. Vinpocetine improves neuronal plasticity and reduces the release of inflammatory cytokines and chemokines from endothelial cells, vascular smooth muscle cells, macrophages, and microglia, by inhibiting the inhibitor of the NF-κB pathway. This review clarifies the anti-inflammatory role of vinpocetine in atherosclerosis and ischemic stroke.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Chemical structure of vinpocetine.
Figure 2
Figure 2
Vinpocetine inhibits the progression of atherosclerosis through the inhibition of IKK/NF-κB. Nuclear factor κ-light-chain-enhancer of activated B cells κB (NF-κB) is a protein complex that controls DNA transcription. It is a major transcription factor that regulates the genes responsible for both the innate and adaptive immune responses. In its inactive state, NF-κB is present in the cytoplasm, attached to the inhibitor of IκB kinase (IKK). When activated by inflammatory signals, the IKK complex phosphorylates and thus activates the inhibitor of κB (IκB). When IκB does not bind to specific DNA sequences (called response elements) to regulate translation, NF-κB is activated and translocates into the nucleus. This results in the triggering of adhesion molecules and cytokines, such as interleukin (IL)-1, IL-2, IL-6, and tumor necrosis factor-α, as well as the activation of chemotaxis. Vinpocetine inhibits the expression of vascular cell adhesion molecule-1 and the E- and P-selectins through the inhibition of NF-κB in endothelial cells, resulting in reduced blood leukocyte attraction and recruitment. By inhibiting monocyte chemoattractant protein-1 production in endothelial cells, vinpocetine affects transformation of monocytes into macrophages, thus further reducing the production of proinflammatory factors through IKK in macrophages. Vinpocetine reduces the expression of growth factors in endothelial cells, which then suppresses the migration and proliferation of vascular smooth muscle cells. This inhibition on VSMCs proliferation and migration occurs through the phosphorylation inhibition of platelet-derived growth factor-BB-induced extracellular signal-regulated protein kinases 1 and 2, and by inhibiting IKK-induced proinflammatory factor production.
Figure 3
Figure 3
Vinpocetine inhibits the progression of stroke through the inhibition of IKK/NF-κB. Vinpocetine inhibits the expression of vascular cell adhesion molecule-1 and the E- and P-selectins through the inhibition of nuclear factor κ-light-chain-enhancer of activated B cells κB (NF-κB) in endothelial cells. This action protects the blood-brain barrier and reduces blood leukocyte attraction and recruitment. Vinpocetine protects neurons by inhibiting voltage-sensitive sodium channels and inhibiting cellular Ca2+ accumulation, which can lead to cell swelling and damage. Damaged neurons release danger-associated molecular patterns, which activate microglia and macrophages through Toll-like receptor 4 activation in the NF-κB pathway. Vinpocetine hinders this process by inhibiting inflammatory cytokine release and magnification. Although vinpocetine does not affect the activation of microglia, it inhibits the proliferation of microglia through NF-κB and the activator protein-1 transcription factors, which are major transcription factors that regulate the genes responsible for both the innate and adaptive immune responses and are important in the differentiation of T cells.
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