Abstract
Background: Garcinia kola (GK) has been experimentally tested for its potential usefulness against oxidative stress-related disorders in a number of body tissues, as well as a number of pathogenic and parasitic diseases. Studies investigating GK extracts’ usefulness in combating nervous tissue toxicity, neuroinflammatory disorders, and neuronal degeneration are still inadequate and not yet conclusive. Purpose: To evaluate the effects of 3,4-methylenedioxymethamphetamine (MDMA)-induced neuroinflammation on the pyramidal neurons and astrocytes of the cornu ammonis 1 (CA1) region of the hippocampus and the role of GK extract (GKE) in attenuating the effects in the rat model. Methods: The study was carried out by using 60 healthy adult male Wistar rats, which were randomly assigned into six groups, A, B, C, D, E, and F (n = 10)—A (control), B (100 mg/kg body weight of GKE only), C (200 mg/kg body weight of GKE only), D (20 mg/kg body weight of MDMA only), E (100 mg/kg body weight of GKE and 20 mg/kg body weight of MDMA), and F (200 mg/kg body weight of GKE and 20 mg/kg body weight of MDMA). Treatment was given for 21 days. Following 24 hours after the last administration, five rats in each group were anesthetized with diether and perfused intracardially, and the brains were excised and fixed in 10 percent neutral buffered formalin for the histological hematoxylin and eosin (H&E) and immunohistochemical glial fibrillary acidic proteins (GFAP). A thin-slice coronal section of the brain was obtained at the level of the optic chiasma and processed via the paraffin-embedding method. Also, the remaining five brains were used to assess neurotransmitter levels (serotonin and dopamine) and cytochrome c-oxidase. The statistical analysis was done using a oneway analysis of variance (ANOVA). Results: A significant reduction (P < .05) in body weight was observed in the group that was administered with MDMA when compared with the control and the rest of the treated groups. Dopamine and serotonin levels were significantly decreased (P < .05) in the MDMA-only group when compared with the control and the rest of the treated groups. The control group and groups B, C, and F showed intact pyramidal neurons, unlike group D, which showed vacuolated and degenerating neurons. The expressions of vacuolation and degeneration in group D were less than those in group E, which received a low dose of GKE and MDMA. Hippocampal astrocytic expressions were significantly higher (P > .05) in the MDMA-only group when compared with the control and other groups. Conclusion: GKE has significant neuroprotective potential against MDMA-induced toxicity in brain tissue. This is evident in its prevention of MDMA-induced oxidative stress, pyramidal neuronal vacuolation, dispersion, and reactive astrogliosis in the CA1 region of the hippocampus. Our findings are dosedependent, with 200 mg/kg of the extract being novel. We, however, recommend further study into the mechanism of action of GKE, on how it attenuates the astrocytic reaction caused by MDMA exposure.
