Saikosaponin B2 modulate oxidative stress in scopolamine induced murine model of Alzheimer’s Disease

Abstract

One of the initial pathological hallmarks of Alzheimer's disease is cognitive decline and memory loss by disruption of cholinergic neurons and oxidative brain damage. A postsynaptic muscarinic receptor blocker, scopolamine impairs cholinergic transmission and impairs cognition. Here, we observed the physiological processes underlying Saikosaponin b2's impact on memory deficits in mice that had been given scopolamine repeatedly. Scopolamine (1 mg/kg) administration for 15 days caused severe deficits in working and short-term memory in mice, as determined by the elevated plus maze, Morris water maze, and novel object recognition tests. However, scopolamine administered mice who were additionally given Saikosaponin b2 did not experience either deficit. This effect was associated with an increase in antioxidant enzymes (superoxide dismutase, Glutathione reductase, glutathione s transferase and catalase), followed by reduction in lipid peroxidation and myeloperoxidase activity.