INVOLVEMENT ARACHIDONIC ACID CASCADE IN MEMORY IMPAIRMENT BY KRATOM (MITRAGYNA SPECIOSA (KORTH.)HAVIL.) IN MALE WISTAR RATS

• Main Author: Aulia Ramadhani, Chelsea
• Format: Theses
• Language: Indonesia
• Online Access: https://digilib.itb.ac.id/gdl/view/82471
• Institution: Institut Teknologi Bandung

Kratom (Mitragyna speciosa (Koth.)Havil.) is a plant that is widely distributed in Southeast Asia, including Indonesia. Recently, mitragynine, the main alkaloid of kratom, has been reported to cause addiction and to impair memory in animals. However, the mechanism by which it reduces memory is still uncleas. The objective of this study is to investigate the potential involvement of the arachidonic acid pathway in memory impairment caused by kratom. To this end, diclofenac will be administered prior to kratom administration. This study employed male Wistar rats, which were divided into seven groups. The first group received a vehicle (CMC Na 0.5%; oral), the second group received kratom leaf ethanol extract (50, 100, and 200 mg/kg BW; oral), and the third group received diclofenac sodium (5 mg/kg BW; intraperitoneal) 30 minutes before the administration of kratom leaf ethanol extract (50, 100, and 200 mg/kg BW; oral) for 14 days. During the 10th to 16th days of the study, spatial learning and memory examintaion were conducted using the Morris Water Maze. On the 17th day, spatial working memory was evaluated using the Y-maze. Subsequently, hippocampal IL-1?levels were observed. Additionally, the profile of the number of microglia and the extent of neuron damage in the CA1 area of the hippocampus were observed. Administration of kratom was demonstrated to result in a reduction in spatial memory and spatial working memory, accompanied by an increase in IL-1?levels within the hippocampus when compared to the vehicle group (P < 0.05). The profile of neuronal damage and the number of microglia in the CA1 area of the hippocampus demonstrate that kratom is associated with increased damage and microglia numbers. Diclofenac sodium was found to prevent the deterioration of spatial memory and working memory, as well as to reduce IL-1?levels in the hippocampus, when compared with the group that received kratom at an equivalent dose (P < 0.05). In the group that received diclofenac sodium pre-treatment, the profile of neuronal damage and the number of glial cells were found to be significantly lower than in the group that only received kratom.