Evaluation of the Effects of Honey on Lipopolysaccharide-Induced Depressive-Like Behavior and Oxidative Stress in Swiss Mice.

Abstract

Depression constitutes over 12.3% of the global disease burden. Recent evidence has suggested oxidative stress as one of the major culprits in the neuropathology of depression as the monoamine theory is now known to be insufficient to account for the pathogenesis of the illness. Honey has been documented to be rich in phenolic compounds and flavonoids, which are potent antioxidants. Hence, this study was designed to examine the potential of honey in the prevention of oxidative stress and depressive-like behaviour in a lipopolysaccharide-induced mouse model of depression.

Thirty Swiss male mice, assigned into 6 groups (n=5), were used for this study. Group 1 received normal saline only while Group 2 received lipopolysaccharide, LPS (830 µg/kg) only. Groups 3-5 were pre-treated with honey (50, 100, and 200 mg/kg) for 7 days plus LPS (830 µg/kg) on the 7th day. Group six received imipramine (10 mg/kg) for seven days plus LPS (830 µg/kg) on the 7th day. The animals were then subjected to behavioural assessment and sacrificed with their brain harvested for lipid peroxidation (MDA) and glutathione (GSH) evaluation on the 8th day. Honey (50, 100, 200 mg/kg) significantly (p < 0.05) reduced the LPS-induced increase in immobility time in the forced swimming test, tail suspension test, and increased the number of lines crossed compared to the LPS-induced decrease in the number of lines crossed in LPS-treated only mice in the open field test. Honey significantly suppressed MDA levels when compared to the LPS-treated only treated mice. Honey protected the brain against lipopolysaccharide-induced behavioural despair, ambulatory deficits, and lipid peroxidation associated with depressive-like behaviours.