Objective: Nootropic activity of Ajuga bracteosa herb was investigated using scopolamine induced amnesia (memory deficits), elevated plus-maze (EPM) and Morris water maze (MWM) experimental models in Swiss albino mice.
Materials and Methods: Successive maceration of the plant was made using n-hexane followed by methanol solvent to extract out active principles according to their solubility. Methanolic herbal extract of Ajuga bracteosa (ABE) was prepared using maceration. Neuroprotective effect of ABE in Swiss albino mouse was recorded in transfer latency time (TLT) as inflation-ratio in EPM, escape latency time (ELT) and time spent in target quadrant (TSTQ) in MWM model using scopolamine induced amnesia. Drug induced lipid per-oxidation was measured by estimation of the content of acetyl cholinesterase (AChE), glutathione (GSH), malondialdehyde (MDA) and total protein in brain blood sample of the mouse.
Results: ABE (500 and 750 mg/kg, p.o.) increased the TLT, ELT and TSTQ. Scopolamine markedly decreased the TLT over 3 minutes, ELT, TSTQ over 90 sec and consecutively impaired learning and memory. Higher levels of brain AChE and MDA but lower levels of brain GSH and total protein were significantly attenuated by chronic administration of ABE herb in scopolamine treated mice at higher doses. The herb improves learning and memory of scopolamine-induced amnesia in mice.
Conclusion: Reversal of scopolamine induced amnesia by ABE may be mediated through the inhibition of oxidative stress and due to presence of withanolides containing anti-cholinesterase activity. ABE may be beneficial in management of memory deficits with normal life and clinical dementia associated with ageing and neurodegenerative states.