Vincamine

Vincamine?is a monoterpenoid indole alkaloid extracted from the?Madagascar periwinkle. Vincamine?is a peripheral?vasodilator?and exerts a selective vasoregulator action on the brain microcapilar circulation^[1]. Vincamine?is a?GPR40?agonist and acts as a β-cell protector by ameliorating β-cell dysfunction and promoting glucose-stimulated insulin secretion (GSIS).?Vincamine?improves glucose homeostasis?in vivo, and has the potential for the type 2 diabetes mellitus (T2DM) research^[2]. In Vitro: Vincamine (20, 40 and 80 μM; 24 hours) exerts a signi?cant, concentration-dependent protective effect in LPS-treated human corneal epithelial cells (HCECs) cells^[1].
Vincamine (20, 40 and 80 μM; 24 hours) significantly reduces ROS level in a dose-dependent manner in LPS-treated human corneal epithelial cells (HCECs)cells. Additionally, ?after Vincamine administration, the levels of MDA is also significantly reduced while the levels of T-AOC, and SOD are increased in a dose-dependent manner^[1].
Vincamine (20, 40 and 80 μM; 24 hours) rescues TrxR activity in a dose-dependent manner in HCECs. However, the intracellular activities of Trx, GR and GPx are neither inhibited nor activated by both LPS and Vincaminer^[1].
Vincamine could activate GPR40 (EC₅₀=6.28?μM) with DHA (GPR40 ligand) as a positive control (EC₅₀=3.85?μM) in hGPR40-CHO cells^[2].
In Vivo: Vincamine (intraperitoneal injection; 15 and 30?mg/kg/day; 6 weeks) improves glucose tolerance in type 2 diabetic model mice. It effectively lowers the levels of fasting blood glucose and glycated hemoglobin. At the same time, it ameliorates oral glucose tolerance and elevated glucose-induced plasma insulin concentration without influence on basal insulin secretion?in vivo^[2].<.br>