Vincamine

Eur J Pharmacol. 1989 Mar 29;162(3):387-95.

Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.[Pubmed: 2744076]

METHODS AND RESULTS:
Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of Vincamine on trachealis, however its relaxant effect was more pronounced. The Vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The Vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration.
CONCLUSIONS:
Our results indicate that the contractile and relaxant actions of Vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.

Pharmacogn Mag. 2017 Jan-Mar;13(49):123-128.

Vincamine Alleviates Amyloid-β 25-35 Peptides-induced Cytotoxicity in PC12 Cells.[Pubmed: 28216895 ]

Vincamine is a plant alkaloid used clinically as a peripheral vasodilator that increases cerebral blood flow and oxygen and glucose utilization by neural tissue to combat the effect of aging. The main purpose of the present study is to investigate the influence of Vincamine on amyloid-β 25-35 (Aβ25-35) induced cytotoxicity, to gain a better understanding of the neuroprotective effects of this clinically used anti-Alzheimer's disease drug.
METHODS AND RESULTS:
Oxidative stress was assessed by measuring malondialdehyde, glutathione, and superoxide dismutase (SOD) levels. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis detection was performed using an Annexin-V-FITC Apoptosis Detection Kit. The production of reactive oxygen species (ROS) was determined using an ROS Assay Kit. Western blot detection was carried out to detect the protein expression. Our studies showed that pretreatment with Vincamine could reduce Aβ25-35 induced oxidative stress. Vincamine markedly inhibited cell apoptosis dose-dependently. More importantly, Vincamine increased the phosphatidylinositol-3 kinase (PI3K)/Akt and Bcl-2 family protein ratios on preincubation with cells for 2 h.
CONCLUSIONS:
Above observation led us to assume that one possible mechanism of Vincamine protects Aβ25-35-induced cell death could be through upregulation of SOD and activation of the PI3K/Akt pathway.Vincamine ameliorates amyloid-β 25-35 (Aβ25-35) peptides induced cytotoxicity in PC12 cellsVincamine reduces Aβ 25-35 peptides induced apoptosis of PC12 cellsVincamine activates the phosphatidylinositol-3 kinase/Akt pathwayVincamine up-regulates the superoxide dismutase.