Buchholzia coriacea seed attenuates scopolamine-induced memory impairment in Mice by down-regulating oxidative stress biomarkers.

Background: Amnesia is a common feature of neurodegenerative disorders. The seeds of Buchholzia coriacea have been traditionally employed to treat various diseases, including inflammatory conditions, pain, infections, and neurological disorders.

Objective: This study aimed to investigate the anti-amnesic and antioxidant potentials of methanol extract of Buchholzia coriacea seed (MEBC) in mice.

Methods: Memory impairment was induced with scopolamine at 3 mg/kg, which was administered i.p. Thirty (30) male Swiss mice (23-27 g) were divided into 6 treatment groups (n = 5): vehicle (10 mL/kg), scopolamine (3 mg/kg, i.p.), MEBC (50, 100, 200 mg/kg, p.o.), and donepezil (reference drug 1 mg/kg, p.o.), respectively. Memory function was assessed using the Morris Water Maze Test (MWMT) and the Y-maze Test (YMT). On the 7th day of administration, AchE, MDA, GSH, catalase, and nitrite were estimated to evaluate the neuroprotective action of Buchholzia coriacea via AchE inhibition and antioxidant activity. The hippocampus and prefrontal cortex were grossed for histological analysis.

Results: The scopolamine treatment resulted in a decrease in percentage alternation, whereas mice pre-treated with MEBC prior to scopolamine had increased percentage alternation in YMT. The mean target quadrant time was significantly increased in the mice pretreated with MEBC. During the probe trial, mice administered with scopolamine had increased search error and chance level of time spent in the target quadrant region. However, MEBC pre-treated mice prior to scopolamine administration had increased latency time in the platform region in MWMT. Scopolamine-mediated changes in MDA and catalase activity were significantly attenuated by MEBC. There is an increased neuronal cell count of the hippocampus and prefrontal cortex region in groups treated with MEBC.

Conclusions: The findings suggest that MEBC seems to be a potent neuropharmacological agent against amnesia, and its mechanism(s) might be modulation of lipid peroxidation and oxidative stress activity associated with the Alzheimer type of amnesia.