Effect of tualang honey against KA-induced oxidative stress and neurodegeneration in the cortex of rats

Abstract

Background: Administration of KA on rodents has resulted in seizures, behavioral changes, oxidative stress, and neuronal degeneration on selective population of neurons in the brain. The present study was undertaken to investigate the extent of neuroprotective effect conferred by Malaysian Tualang Honey (TH), an antioxidant agent, in the cerebral cortex of rats against KA-induced oxidative stress and neurodegeneration in an animal model of KA-induced excitotoxicity. Methods: Male Sprague-Dawley rats were randomly divided into five groups: Control, KA-treated group, TH + KA-treated group, aspirin (ASP; anti-inflammatory agent) + KA-treated group and topiramate (TPM; antiepileptic agent) + KA-treated group. The animals were pretreated orally with drinking water, TH (1.0g/kg BW), ASP (7.5mg/kg BW) or TPM (40mg/kg BW), respectively, five times at 12 h intervals. KA (15mg/kg BW) was injected subcutaneously 30 min after last treatment to all groups except the control group (normal saline). Behavioral change was observed using an open field test (OFT) to assess the locomotor activity of the animals. Animals were sacrificed after 2 h, 24 h and 48 h of KA administration. Results: KA significantly inflicted more neuronal degeneration in the piriform cortex and heightened the predilection to seizures as compared with the control animals. Pretreatment with TH reduced the KA-induced neuronal degeneration in the piriform cortex but failed to prevent the occurrence of KA-induced seizures. In the OFT, KA-induced animals showed an increased in locomotor activity and hyperactivity and these were attenuated by TH pretreatment. Furthermore, TH pretreatment significantly attenuated an increase of thiobarbituric acid reactive substances level and a decrease of total antioxidant status level enhanced by KA in the cerebral cortex. Conclusion: These results suggest that pretreatment with TH has a therapeutic potential against KA-induced oxidative stress and neurodegeneration through its antioxidant effect.