CONTEXT: Erythrina velutina (EV) Willd (Fabaceae-Faboideae) is a medicinal tree that is commonly used in Brazil for the treatment of several central nervous system disorders. OBJECTIVE: The anticholinesterase activity of EV is described in this work. METHODS: Concentration-response curves (0-1.6 mg/mL) for EV leaf aqueous extract (AE) and alkaloid-rich extracts (AKEs) were performed in vitro. Cholinesterase inhibition was examined in mouse brains, as the cholinesterase source, and in pure acetylcholinesterase (AChE) or butyrylcholinesterase (BuChE). Mice were treated with AE or AKE (100, 200, and 400 mg/kg, p.o.) and their brains were used for the measurement of cholinesterase activity (CA) ex vivo. RESULTS: CA was inhibited by AE (IC(50) = 0.57 [0.43-0.75] mg/mL) and AKE (IC(50) = 0.52 [0.39-0.70] mg/mL) in brain homogenates in a concentration-dependent manner. The ex vivo experiments indicated that AE (400 mg/kg, p < 0.05, 32.2 ± 3.9% of inhibition) and AKE (all doses: p < 0.05-p < 0.001, 29.6 ± 3.2% as the maximum inhibition) significantly inhibited CA in the central nervous system after oral administration. AE and AKE inhibited AChE and BuChE activities in a concentration-dependent manner (AE: IC(50AChE) = 0.56 [0.38-0.81] mg/mL, IC(50BuChE) = 2.95 [1.51-5.76] mg/mL, AKE: IC(50AChE) = 0.87 [0.60-12.5] mg/mL, IC(50BuChE) = 2.67 [0.87-8.11] mg/mL). DISCUSSION AND CONCLUSIONS: These data indicated that AE and AKE crossed the blood-brain barrier to inhibit CA in the brain. AE and AKE also exhibited a dual inhibitory action on acetyl- and BuChE.
CONTEXT: Erythrina velutina (EV) Willd (Fabaceae-Faboideae) is a medicinal tree that is commonly used in Brazil for the treatment of several central nervous system disorders. OBJECTIVE: The anticholinesterase activity of EV is described in this work. METHODS: Concentration-response curves (0-1.6 mg/mL) for EV leaf aqueous extract (AE) and alkaloid-rich extracts (AKEs) were performed in vitro. Cholinesterase inhibition was examined in mouse brains, as the cholinesterase source, and in pure acetylcholinesterase (AChE) or butyrylcholinesterase (BuChE). Mice were treated with AE or AKE (100, 200, and 400 mg/kg, p.o.) and their brains were used for the measurement of cholinesterase activity (CA) ex vivo. RESULTS: CA was inhibited by AE (IC(50) = 0.57 [0.43-0.75] mg/mL) and AKE (IC(50) = 0.52 [0.39-0.70] mg/mL) in brain homogenates in a concentration-dependent manner. The ex vivo experiments indicated that AE (400 mg/kg, p < 0.05, 32.2 ± 3.9% of inhibition) and AKE (all doses: p < 0.05-p < 0.001, 29.6 ± 3.2% as the maximum inhibition) significantly inhibited CA in the central nervous system after oral administration. AE and AKE inhibited AChE and BuChE activities in a concentration-dependent manner (AE: IC(50AChE) = 0.56 [0.38-0.81] mg/mL, IC(50BuChE) = 2.95 [1.51-5.76] mg/mL, AKE: IC(50AChE) = 0.87 [0.60-12.5] mg/mL, IC(50BuChE) = 2.67 [0.87-8.11] mg/mL). DISCUSSION AND CONCLUSIONS: These data indicated that AE and AKE crossed the blood-brain barrier to inhibit CA in the brain. AE and AKE also exhibited a dual inhibitory action on acetyl- and BuChE.