Aruncus dioicus var. kamtschaticus extract suppresses mitochondrial apoptosis induced-neurodegeneration in trimethyltin injected ICR mice

In the present study, we attempt to confirm the effect of the ethyl acetate fraction from Aruncus dioicus var. kamtschaticus (EFAD) against neurodegeneration with various experiments using trimethyltin (TMT). First, learning and memory deterioration caused by TMT was examined with several behavioral tests. EFAD had an improvement effect on TMT-induced cognitive dysfunction. Second, to assess the oxidative stress caused by TMT, a series of biochemical indicators of the cholinergic and antioxidant system were measured. EFAD showed superb effects on the recovery of the cholinergic system and reduction of oxidative stress. Third, to identify the mitochondrial apoptosis caused by TMT, mitochondrial activity and mitochondrial apoptotic signaling molecules were analyzed. EFAD improved mitochondrial activity and suppressed mitochondrial apoptosis. Finally, dicaffeoylglucose isomers were identified as main compounds of EFAD with ultra-performance liquid-quadrupole-time-of flight mass spectrometry (UPLC-QTOF/MS2). Consequently, EFAD showed a protective effect against mitochondrial apoptosis-induced neurodegeneration in TMT-injected mice based on antioxidant ability.