Vincamine alleviates amyloid-β 25-35 peptides-induced cytotoxicity in PC12 cells

Abstract

Objective: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.Materials and Methods: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.Results: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.Conclusion: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.SUMMARY 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. Abbreviation used: Aβ25-35: Amyloid-β 25-35; AD: Alzheimer's disease; BCA: Bicinchoninic acid; GSH: glutathione; PBS: Phosphate buffered solution; SDS: Sodium dodecylsulphate; SOD: Superoxide dismutase

Neuroprotective Effect of Piracetam and Vincamine in a Rat Model of Haloperidol-induced Parkinson's Disease

“…Vincamine is claimed to improve memory impairment accompanying neurodegenerative diseases by its antioxidant effect, increasing cerebral blood flow and glucose and oxygen utilization by the neurons [31].…”

Effects of Vincamine on Testicular Dysfunction in Alloxan-induced Diabetic Male Rats

“…Natural components have been demonstrated to play an essential impact in the prevention of human illnesses in epidemiological investigations. Among them, vincamine has been reported to have therapeutic potential for cerebral metabolic and circulatory disorders (21). This paper was the first research about the potential reaction of vincamine on an alloxan-induced diabetic rat with spermatogenic dysfunction.…”

Disease-modifying effects of Vincamine supplementation inDrosophilaand human cell models of Parkinson’s disease

“…Since age-linked ND are characterized by a disturbance in trace element levels in the brain, it was suggested that VIN might exert a beneficial effect in aged people by decreasing OS (Fayed, 2010). It was also shown that VIN was able to reduce Aβ-induced cytotoxicity in PC12 cells by decreasing the concentrations/activities of a variety of OS indicators (Han et al, 2017). As previously reported, DJ-1β mutants exhibited high levels of reactive oxygen species (ROS) and protein carbonylation (a post-translational modification caused by high ROS levels) when compared to control flies (Casani et al, 2013; Lavara-Culebras et al, 2010).…”

“…Since neurodegeneration in PD is the result of the combination of processes occurring inside and/or outside the cells, its etiopathogenesis is not yet completely understood. Despite this, several works suggest that mitochondrial alterations, protein misfolding and aggregation, autophagy defects, inflammation, increased oxidative stress (OS) levels, calcium dyshomeostasis, and metabolic alterations might play an important role in the development of the disease (Anandhan et al, 2017; Groenendyk et al, 2021; Mahmood et al, 2021; Poewe et al, 2017; Solana-Manrique et al, 2022). PD is characterized by a range of motor symptoms such as bradykinesia, resting tremor, rigidity and postural instability.…”