Tualang Honey Reduced Neuroinflammation and Caspase-3 Activity in Rat Brain after Kainic Acid-Induced Status Epilepticus.

Nur Shafika Mohd Sairazi,Mustapha Muzaimi,Swamy Mummedy,Siti Amrah Sulaiman,Mohd Asnizam Asari,Kuttulebbai N S Sirajudeen

doi:10.1155/2018/7287820

Nur Shafika Mohd Sairazi, Mustapha Muzaimi + Show 4 more

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https://doi.org/10.1155/2018/7287820

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Abstract

The protective effect of tualang honey (TH) on neuroinflammation and caspase-3 activity in rat cerebral cortex, cerebellum, and brainstem after kainic acid- (KA-) induced status epilepticus was investigated. Male Sprague-Dawley rats were pretreated orally with TH (1.0 g/kg body weight) five times at 12 h intervals. KA (15 mg/kg body weight) was injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Neuroinflammation markers and caspase-3 activity were analyzed in different brain regions 2 h, 24 h, and 48 h after KA administration. Administration of KA induced epileptic seizures. KA caused significant (p < 0.05) increase in the level of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), glial fibrillary acidic protein (GFAP), allograft inflammatory factor 1 (AIF-1), and cyclooxygenase-2 (COX-2) and increase in the caspase-3 activity in the rat cerebral cortex, cerebellum, and brainstem at multiple time points. Pretreatment with TH significantly (p < 0.05) reduced the elevation of TNF-α, IL-1β, GFAP, AIF-1, and COX-2 level in those brain regions at multiple time points and attenuated the increased caspase-3 activity in the cerebral cortex. In conclusion, TH reduced neuroinflammation and caspase-3 activity after kainic acid- (KA-) induced status epilepticus.

Highlights

Excitotoxicity is the major mechanism of neuronal death [1]
TNFα and IL-1β levels were statistically significantly higher (p
In the cerebral cortex and brain stem was significantly higher (p

Summary

Introduction

Excitotoxicity is the major mechanism of neuronal death [1]. Excitotoxicity is a process triggered by the excessive activation of ionotropic glutamate receptors induced by excessive release of excitatory amino acids, such as glutamate which cause excitotoxic neuronal degeneration and eventually neuronal death. Kainic acid (KA) is a powerful neurotoxic analogue of glutamate and an agonist of kainate subtype of ionotropic glutamate receptors. KA has been extensively used to study the mechanism of excitotoxicityinduced neurodegeneration and to establish the model for epileptic due to the ability of KA to induce neuroinflammation and apoptosis in the brain [2]. KA-induced excitotoxicity is associated with neuroinflammation characterized by activation of microglia and astrocytes and increased level of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-1

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