Vinpocetine is a phosphodiesterase (PDE) inhibitor and inhibits NF-κB-dependent inflammatory responses by directly targeting IκB kinase complex (IKK), and has been widely used for the treatment of cerebrovascular disorders[3]. Vinp inhibits mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB)-dependent inflammatory responses and oxidative damage in which osteoclasts are often involved[4]. In both in vivo and in vitro experiments, vinpocetine can confer protection of rat renal cells by inhibiting the NF-κB signaling pathway and activating the Nrf2/ARE signaling pathway[5]. Vinpocetine potently suppressed tumor necrosis factor-α-induced nuclear factor kappa-light-chain-enhancer of activated B cells activation and proinflammatory mediator expression in primary cultured macrophages in vitro, as well as in the aorta wall in vivo, suggesting vinpocetine conferred anti-AAA (Abdominal aortic aneurysm) effect at least partially via the inhibition of inflammation[6]. Vinpocetine treatment may exhibit anti-inflammatory activity and alleviate cognitive impairment[7]. The effects of vinpocetine might be attributed not only to its antioxidant and anti-inflammatory properties, but also to its suppressing effect on GSK3β (Glycogen synthase kinase-3β) activity and its downstream BACE1(β-secretase) [8].
Vinpocetine/长春西汀 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Primary rat astrocytes
30 µM
12 hours hypoxia/6 hours reoxygenation
Vinpocetine ameliorated oxygen-glucose deprivation/reoxygenation (OGD/R)-induced astrocytic injury via the PI3K/AKT signaling pathway, improving cell viability, reducing LDH release, and decreasing oxidative stress and inflammatory responses.
Front Neurosci. 2020 Apr 2;14:223
Vascular smooth muscle cells (SMCs)
10, 20, 30, 50 µM
16 hours
Vinpocetine dose-dependently inhibited PDGF-stimulated vascular smooth muscle cell migration, as confirmed by two-dimensional migration assays and three-dimensional aortic medial explant invasive assay.
J Pharmacol Exp Ther. 2012 Nov;343(2):479-88
Adult mouse cardiac fibroblasts
10 µM
24 hours
Vinpocetine suppressed TGFβ-induced fibroblast activation and extracellular matrix gene expression
Cardiovasc Drugs Ther. 2017 Apr;31(2):157-166
Vascular smooth muscle cells (SMCs)
25, 50, 75 µM
24 hours
Vinpocetine dose-dependently inhibited vascular smooth muscle cell proliferation, causing G1-phase cell cycle arrest, associated with a decrease in cyclin D1 and an increase in p27Kip1 levels.
J Pharmacol Exp Ther. 2012 Nov;343(2):479-88
BV2 cells
20 µM
24 hours
Vinpocetine inhibits OGD-induced M1 phenotype and promotes M2 phenotype in BV2 cells
Front Cell Dev Biol. 2021 Feb 4;8:616590
MRC-5 cell line
100, 50, 25, 12.5, 6.25 mcg/mL
24-48 hours
To assess the cytotoxicity of vinpocetine on the MRC-5 cell line, results showed that vinpocetine exhibited low cytotoxicity against MRC-5 cells with an IC50 of 289.2 µg/ml.
Sci Rep. 2024 May 15;14(1):11131
Mouse resident peritoneal macrophages
30 µM
30 minutes or 6 hours
Vinpocetine suppressed TNF-α-induced p65 nuclear translocation and proinflammatory mediator expression
Clin Sci (Lond). 2020 Nov 27;134(22):2959-2976
MRC-5 cell line
100 µg/mL
48 hours
Vinpocetine significantly reduced the expression of fibrotic genes (fibronectin, vimentin, α-SMA, and Smad2/3) induced by TGF-β1, indicating its anti-fibrotic effect by interfering with the TGF-β1/Smad signaling pathway.
Sci Rep. 2024 May 15;14(1):11131
Human middle ear epithelial cells (HMEEC)
10 µM
6 hours
Vinpocetine inhibited S. pneumoniae-induced upregulation of pro-inflammatory mediators (IL-1β, IL-6, IL-8, and TNF-α) mRNA expression
Proc Natl Acad Sci U S A. 2010 May 25;107(21):9795-800
Adult mouse cardiomyocytes
10-40 µM
72 hours
Vinpocetine dose-dependently suppressed Ang II-stimulated myocyte hypertrophic growth
Cardiovasc Drugs Ther. 2017 Apr;31(2):157-166
ARPE19/NF-κB-luciferase reporter cells
50 µM
8 hours
To evaluate the inhibitory effect of vinpocetine on Aβ-induced NF-κB activation. Results showed that vinpocetine significantly suppressed Aβ-induced NF-κB activation, reducing it to a level comparable to the control group.
Exp Eye Res. 2014 Oct;127:49-58
Vinpocetine/长春西汀 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Wistar rats
High-fructose diet-induced metabolic syndrome model
Tube feeding
1 mg/kg
From the ninth week, lasting for 12 weeks
To investigate the ameliorative effect of Vinpocetine on metabolic syndrome-associated bladder overactivity, results showed that Vinpocetine restored the contraction and relaxation responses of bladder detrusor muscle and exerted anti-inflammatory effects.
Biomedicines. 2022 Oct 26;10(11):2716
Sprague Dawley rats
High-fat diet (HFD) and diabetes-induced fatty liver model
Oral
10 and 20 mg/kg/day
Once daily for 8 weeks
Vinpo dose-dependently mitigated the HFD-induced rise in serum ALT, AST, and ALP activities and improved the hepatic architecture of steatotic rats, especially at a dose of 20 mg/kg. The findings elucidated the mechanisms behind Vinpo's beneficial effects, including insulin sensitivity improvement, attenuation of oxidative stress, and dampening of the sterile inflammatory response. The concomitant administration of Lactobacillus spp. probiotics with Vinpo significantly enhanced these effects.
AMB Express. 2024 Aug 2;14(1):89
Wistar rats
Middle cerebral artery occlusion (MCAO) model
Intraperitoneal injection
10 mg/kg
Single dose, 30 min before MCAO
Vinpocetine activated the PI3K/AKT signaling pathway to enhance phosphorylation of astrocytic connexin 43 (Cx43), thereby attenuating cerebral ischemia/reperfusion injury, reducing cerebral infarction volume and edema, and decreasing oxidative stress, inflammation, and apoptosis.
Front Neurosci. 2020 Apr 2;14:223
Mice (C57BL/6)
S. pneumoniae-induced otitis media model
Intraperitoneal injection
10 mg/kg
Post-infection treatment at 2 hours, continued for 3 days
Vinpocetine significantly suppressed S. pneumoniae-induced middle ear inflammation, including upregulation of inflammatory mediators, mucosal thickening, and neutrophil infiltration
J Immunol. 2020 Feb 15;204(4):933-942
Female Wistar albino rats
Estradiol-benzoate induced cervical hyperkeratosis model
Oral
10 mg/kg/day
Once daily for 4 weeks
Vinpocetine significantly alleviated all biochemical and histopathological abnormalities induced by EB, mitigating cervical hyperkeratosis via NLRP3-induced pyroptosis and activation of the SIRT1/Nrf2 signaling pathway.
Sci Rep. 2024 Aug 19;14(1):19171
Adult Long-Evans rats
Aβ-induced retinal inflammation model
Intraperitoneal injection
15 mg/kg
Once daily for four days
To evaluate the inhibitory effect of vinpocetine on Aβ-induced NF-κB nuclear translocation and inflammatory responses. Results showed that vinpocetine significantly inhibited NF-κB nuclear translocation and reduced the expression and activation of NLRP3, caspase-1, IL-1β, IL-18, and TNF-α.
Exp Eye Res. 2014 Oct;127:49-58
Mice
LPS- or TNF-α-induced lung inflammation model
Intraperitoneal injection
2.5, 5, 10 mg/kg
Single dose, lasting 6 h
Vinpocetine dose-dependently inhibited LPS- or TNF-α-induced inflammatory mediator expression and neutrophil infiltration
Proc Natl Acad Sci U S A. 2010 May 25;107(21):9795-800
Male albino rats
Aluminum-induced Alzheimer's disease model
Oral
20 mg/kg
Daily for five weeks
Vinpocetine in combination with cocoa significantly improved cognitive function and behavioral performance in the aluminum-induced Alzheimer's disease model, reduced oxidative stress and inflammation, and modulated the Wnt/β-catenin/GSK-3β/Nrf2/HO-1 and PERK/CHOP/Bcl-2 pathways.
Pharmaceutics. 2023 Jul 31;15(8):2063
BALB/c male mice
Bleomycin-induced pulmonary fibrosis model
Oral
20 mg/kg/day
Once daily from day 7 of induction till the end of the experiment (day 21)
Vinpocetine significantly alleviated bleomycin-induced fibrotic endpoints, including reduced expression of fibrotic-related proteins, oxidative stress, and inflammatory mediators, and exerted anti-fibrotic effects by upregulating Nrf2 and PPAR-γ expression and downregulating the NLRP3/NF-κB pathway.
Sci Rep. 2024 May 15;14(1):11131
Wistar rats
Adenine-induced chronic kidney disease model
Oral
20 mg/kg/day
Daily administration for 4 weeks
Vinpocetine ameliorated adenine-induced renal fibrosis and epithelial-mesenchymal transition by targeting the DNMT1/Klotho/β-catenin/Snail1 and MMP-7 pathways
Ang II-induced cardiac hypertrophy and fibrosis model
Intraperitoneal injection
5 mg/kg/day
Once daily for 17 days (3 days prior and 14 days during Ang II infusion)
Vinpocetine significantly attenuated Ang II-induced cardiac hypertrophy and fibrosis
Cardiovasc Drugs Ther. 2017 Apr;31(2):157-166
FVB/NJ mice
Carotid artery ligation injury model
Intraperitoneal injection
5 mg/kg/day
Once daily for 14 days
Vinpocetine significantly reduced neointimal formation after carotid artery ligation injury and decreased spontaneous remodeling of human saphenous vein explants.
United States, California
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Stanford University
Recruiting
Palo Alto, California, United States, 94304
Contact: Jordan Seliger 650-468-8740 jseliger@stanford.edu
Principal Investigator: Kimford J Meador, MD 收起 <<
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