Zulkifli, Nurdarina Ausi
(2021)
Effects of tualang honey on kainic acid-induced morphological changes and glutamate transporter (EAAT2) expression in the cerebellum and striatum of rats.
Masters thesis, Universiti Sains Malaysia.
Abstract
Excitotoxicity is a type of neuronal cell death induced by excessive glutamate
or other excitatory amino acids and has been implicated in various neurodegenerative
diseases. The excitatory amino acid transporter 2 (EAAT2) is a major glutamate
transporter responsible for nearly 90% of glutamate reuptake in the brain. Loss of
EAAT2 causes accumulation of extracellular glutamate and excitotoxicity. Tualang
honey (TH) is a Malaysian honey that has shown many beneficial effects in various
disease models. The main objectives of this study were to evaluate the potential
protective effects of Tualang honey on kainic acid-induced morphological changes and
EAAT2 expression in the cerebellum and striatum of rats. A total of 48 male adult
Sprague Dawley rats with the weight of 260-320g were randomly divided into four
major groups (n = 12 per group) depending on the treatment received: control, KA,
TH+KA and TPM+KA. Each major group was further divided into two subgroups
depending on sacrifice time (24 hours or 5 days following KA administration) (n = 6
per subgroup). The rats were pre-treated orally with distilled water (groups control and
KA), Tualang honey (1.0 g/kg; group TH+KA) or topiramate (40 mg/kg; group
TPM+KA) for five times at 12 hours interval. The rats were then injected
subcutaneously with KA (15 mg/kg; groups KA, TH+KA and TPM+KA) or normal
saline (control) 30 minutes after the last oral treatment. An open field test was
performed to assess the locomotor activity of rats before the rats were sacrificed at 24
hours or 5 days after the KA administration. The cerebellum and striatum were
collected for histological and EAAT2 assessment. Significant reduction in the number of viable neurons and EAAT2 expression were observed in both cerebellum and
striatum 24 hours following KA administration. KA-induced significant increase in
locomotor activity, along with significantly reduced viable neurons in the cerebellum
and EAAT2 expression in the striatum were observed 5 days following KA
administration. Pre-treatment with TH increased the number of viable neurons and
EAAT2 expression in the cerebellum and striatum. The effects were comparable to
TPM, the control drug used in this study. These findings suggest that pre-treatment
with TH showed some protective effects against KA-induced excitotoxicity via
modulation of EAAT2 expression.
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