Inhibited Brain Acetylcholinesterase Activity Research Articles

Anti-Amnesic Effect of Curculigo orchioides Plant Extract and Its Function on Acetylcholinesterase Enzyme

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, and one of the most predominant causes of dementia in older people. Preventing acetylcholine from breakdown by an excess amount of acetylcholinesterase is a proven therapy for AD. Traditionally Curculigo orchioides is known for its antioxidant activity, enzyme inhibition activity, and other medicinal uses. In this study, in vitro acetylcholinesterase, inhibitory activity was investigated, and methanolic extract of the plant showed significant activity. This study aims to investigate cholinesterase inhibitory activity, learning, and memory-enhancing activity of Curculigo orchioides.
 Materials and Methods: The crude methanol extract of the dried powder was prepared by the cold extraction method. In-vitro acetylcholinesterase (AChE) inhibitory activities were determined by the modified Ellman’s method. To confirm learning and memory-enhancing effects, the scopolamine-induced memory impairment Swiss-albino mice were used, and to find the anti-amnesic effect of the extract, a passive shock avoidance task was applied.
 Results: Results proved that scopolamine-induced cognitive dysfunction decreased significantly by administration of the plant extract solution in the passive avoidance task, and inhibited brain acetylcholinesterase activity. While running an in-vitro AChE inhibitory test the IC50 was 0.782±0.067μg/ml.
 Conclusion: The results suggested that methanolic extract of Curculigo orchioides can inhibit AChE in-vitro. Besides this, it provides data that proves its ability to improve whole brain AChE activity and enhance memory.

Bone Strength and Acetylcholinesterase Inhibition as Endpoints in Chlorpyrifos Toxicity toFundulus heteroclitus

Brain acetylcholinesterase (AChE) inhibition was measured during 4-week and 4-day episodic exposures to chlorpyrifos. Organisms were exposed to a seawater (−) control, an acetone (+) control (0.1%), and 0.625, 1.25, 2.5, 5.0, and 10.0 μg of chlorpyrifos L−1in each test. These episodic exposures significantly depressed AChE activity at 2.5, 5.0, and 10.0 μg L−1(weekly test) and at 1.25, 2.5, 5.0, and 10.0 μg L−1(daily test). Six-hour pulsed exposure to chlorpyrifos inhibited brain AChE activity at concentrations as low as 1. 25 μg L−1. Stress at failure of caudal vertebrae following episodic exposure was also tested. Analysis of samples from daily 6-h treatments found no differences after 2 days; however, vertebrae were significantly weaker (than controls) after 4 days. Analysis of weekly 6-h exposures found weaker caudal vertebrae after 2 weeks but not after 4 weeks.

Feeding behavior and brain acetylcholinesterase activity in bream ( Abramis brama L.) as affected by DDVP, an organophosphorus insecticide

1. Bream ( Abramis brama) were exposed to sublethal concentration of organophosphorus insecticide DDVP and the amount of food consumed and brain acetylcholinesterase (AChE) examined in exposed fish. 2. Exposure to DDVP resulted in decreased amount of food consumed and inhibited brain AChE activity. 3. Intraperitoneal injection of the fish with cholinergic drugs, atropine and TMB-4 recovered the feecling efficiency in exposed fish. TMB-4 recovered brain AChE activity as well. 4. The results revealed that cholinergic system in fish brain constitutes biochemical mechanism controlling feecling behavior in fish.

An irreversible anticholinesterase probe for studying increased permeability of the rat blood-brain barrier

Phospholine iodide, a potent anticholinesterase quarternary salt, was found to be a useful probe in studying changes in blood-brain barrier permeability in rats exposed to various insults. Based on brain acetylcholinesterase (AChE) activity measurements, it was concluded that phospholine iodide, injected i.m. at a dose of 65 μg/kg, inhibited brain AChE activity in three different regions, provided that the blood-brain barrier integrity was damaged by exposing rats to osmotic shock (glycerol), convulsions (metrazole), or γ-irradiation. Enzyme activity was not inhibited in sham-handled controls treated with phospholine iodide. Possible complication from blood contamination during brain processing was ruled out. It was suggested that phospholine iodide can be used as a semi-quantitative probe to detect an increase in blood-brain barrier permeability by the establishment of a unidirectional flow of the marker from brain capillaries into extravascular spaces and the phosphorylation of brain AChE. Based on the stability of the inhibited AChE and its 100 per cent reactivability in the presence of specific nucleophiles, this probe may be useful for the study of blood-brain barrier resistance in conscious, freely moving rats exposed to various stresses.