Neuroprotective effect of biatractylenolide against memory impairment in D-galactose-induced aging mice.

Biatractylenolide, a sesquiterpene lactone, which exerted the neuroprotective effect against glutamate-induced excitotoxicity, was isolated from Atractylodis macrocephala in our previous study. In this study, we evaluated the neuroprotective effect of biatractylenolide against D-galactose-induced memory impairment and explored the potential mechanism of its action. The results showed that administration of biatractylenolide could significantly improve behavioral performance of D-galactose-treated mice in passive avoidance test and spatial learning-memory test. Administration of biatractylenolide could significantly decrease the formation of reactive oxygen species (ROS), decrease the activity of acetylcholinesterase (AChE), and increase the expression of synapsin I and protein kinase C (PKC) in D-galactose-treated mice. Our findings provide first evidence for the neuroprotective effect of biatractylenolide against D-galactose-induced memory impairment. The potential mechanisms underlying the neuroprotective effect of biatractylenolide in D-galactose-treated mice might be (i) attenuating oxidative damage via decreasing ROS formation, (ii) restoring cholinergic neurotransmission via decreasing AChE activity, and (iii) increasing the expression of memory-related proteins (synapsin I and PKC). Biatractylenolide may have therapeutic potential in aging-related memory impairment.