Pre-treatment of Diclofenac Prevents Memory Impairment After Mitragyna speciosa (Korth.) Havil. Administration: Role of the Arachidonic Acid Cascade

Mitragyna speciosa (MS) has been reported to cause memory impairment, and early studies suggest the involvement of the arachidonic acid cascade in cognitive disorders. This study was conducted to investigate the potential of diclofenac pre-treatment to prevent memory impairment caused by MS. Male Wistar rats were divided into five groups: vehicle group (CMC Na 0.5%; p.o), mitragynine ethanolic extract (MSEE) groups (50 and 100 mg/kg BW; p.o), and the MSEE groups pretreated with diclofenac sodium (5 mg/kg BW; i.p). The treatments were given for two weeks. The memory performances were evaluated using MWM and Y-maze tests. The changes in IL-1β level, profiles of the microglia, and degenerated neurons in the hippocampal CA1 were observed. The administration of MSEE was demonstrated to impair memory in behavioral tests, accompanied by an increase in IL-1β levels in the hippocampus compared to the vehicle group (P<0.05). Histological examination revealed increased numbers of microglia and degenerated neurons after MSEE. Pre-treatment of diclofenac significantly improved (P<0.05) the memory performance as well as IL-1β levels and ameliorated the histological presentation. The results of the present study indicate the essential of the arachidonic acid cascade in MS-induced memory impairment.