Hasim, Hidani
(2023)
Characterisation of tualang honey silver nanoparticles (THSN) and neuroprotective effect of tualang Honey and thsn on kainic acid-induced neurodegeneration in male rats’ hippocampus.
Masters thesis, Universiti Sains Malaysia.
Abstract
Neurodegeneration is a feature of many chronic disorders of the central
nervous system that result in the deterioration of neuronal structure and function.
Experimental induction of excitotoxicity-mediated neurodegeneration by kainic acid
(KA) has been associated with various mechanisms, including oxidative stress,
excessive inflammatory response, and apoptosis. Tualang honey (TH), which
contains a powerful natural antioxidant, is increasingly studied as an alternative
prevention for several neurodegenerative diseases. Despite the numerous studies
highlighting the benefits of TH, the application of silver nanoparticles synthesised
from TH remains limited. Thus, this research aimed to evaluate the neuroprotective
effects of TH and TH silver nanoparticles (THSN) against KA-induced
neurodegeneration in the rat hippocampus. THSN was synthesised and characterised
by UV-Visible (UV-Vis) spectroscopy, X-ray Diffraction (XRD), Fourier Transform
Infrared (FTIR) spectroscopy, Field Emission Scanning Electron Microscope
(FESEM), and Transmission Electron Microscope (TEM). A total of 288 male
Sprague Dawley rats were randomised into three experimental phases (including
behavioural assessment, biochemical measurement, and histological studies). In each
phase, 96 rats were randomly divided into eight major groups (n = 12/major group):
control, THSN 10 mg, THSN 50 mg, KA only, KA + TH, KA + THSN 10 mg, KA +
THSN 50 mg, and KA + Topiramate (TPM). Each major group was subdivided into 24h and five days subgroups, comprising 16 subgroups (n = 6/subgroups). The rats were given distilled water, TH (1.0 g/kg), THSN (10 mg/kg or 50 mg/kg), or TPM
(40 mg/kg) orally, five times at 12 h intervals. Subcutaneous injections of saline
solution or KA (15 mg/kg) were given 30 min after the last oral treatments. Before
the animals were euthanised, behavioural assessments were conducted using the open
field test and a novel object recognition test. Biochemical, toxicological, and
histological analyses were performed on the hippocampus at 24 h and 5 days
following KA induction. The KA administration on rats resulted in seizures,
alteration in locomotor activity, and memory impairment. Additionally, KA
increased oxidative stress (as evidenced by significant increases in MDA, PCO, and
NOx levels and significant decreases in CAT, SOD, GSH and TAS levels), TNF-α
level (neuroinflammatory marker), caspase-3 activity (apoptosis marker), and
subsequent neurodegeneration in the hippocampus. The result for renal and liver
function test showed that THSN caused no significant toxic effect on animals.
Notably, TH and THSN pre-treatment increased the seizure latency, improved
memory deficits, and reduced oxidative stress, neuroinflammation, apoptosis, and
neuronal damage of rats’ hippocampus in the KA-induced neurodegeneration model.
In conclusion, TH and THSN exerted their neuroprotective effects against KA-induced
neurodegeneration via antioxidant, anti-inflammatory, and anti-apoptotic
properties. Further clinical studies need to be conducted to establish TH and THSN
as a potential neuroprotective agent.
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