ANTIMALARIAL EFFECTS OF GABAPENTIN IN MICE WITH CEREBRAL MALARIA AND ITS MOLECULAR DOCKING ANALYSIS WITH CLUSTER OF DIFFRENTIATION 36 AND 47

Background: Cerebral malaria caused by Plasmodium falciparum is one of the most severe forms of malaria, often leading to death or long-term neurological problems. Current treatments mainly clear parasites but do not fully protect the brain. Drug repurposing offers a faster way to find new therapies. Gabapentin, widely used for epilepsy and neuropathic pain, has shown neuroprotective properties, but its potential role in cerebral malaria has not been studied. Aim: This study aimed to investigate the antimalarial and neuroprotective effects of gabapentin in mice infected with Plasmodium berghei ANKA and to explore its possible interactions with CD36 and CD47 receptors through molecular docking. Methodology: A total of 80 Swiss albino mice were randomly divided into eight groups, including untreated, artesunate-treated, and gabapentin-treated groups at different doses (75 mg/kg, 150 mg/kg, and 300 mg/kg). Survival, parasitemia, body weight, body temperature, and neurological signs were monitored over 28 days. Molecular docking was performed using AutoDock Vina to predict the binding of gabapentin with CD36 and CD47. Results: Gabapentin improved survival, lowered parasitemia, and alleviated neurological symptoms in infected mice, with the highest dose showing the strongest effect, though less than artesunate. It also stabilized body weight and temperature. Docking analysis suggested possible binding of gabapentin to CD36 and CD47. Conclusion: Gabapentin shows promise as a repurposed adjunctive therapy for cerebral malaria by improving survival and neurological outcomes in mice, while also demonstrating potential molecular interactions with key host receptors. Further studies are needed to confirm these findings in humans.