The effect of ghrelin on antioxidant status in the rat’s model of Alzheimer's disease induced by amyloid-beta

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder associated with amyloid-beta (Aβ) plaque formation and oxidative stress in the brain. Ghrelin has been proven to exert antioxidant activity and neuroprotection in different neurological diseases. This study is going on to examine the effect of ghrelin on antioxidant status in the rat’s model of AD induced by Aβ. Cognitive impairment was induced by intra-hippocampal administration of Aβ (10 μg) in Wistar rats and ghrelin (80 μg/kg) was administrated intraperitoneal for ten consecutive days. Behavior was assessed with Morris water maze and passive avoidance tests. Malondialdehyde (MDA) level as a marker of lipid peroxidation was assessed using the thiobarbituric acid. Catalase activity was assayed by the decomposition of H 2 O 2 . Antioxidant capacity was determined using the FRAP method. Treatment with ghrelin decreased the hippocampus and serum MDA levels in wild-type rodents and prevented an increase in hippocampal and serum MDA levels in animals receiving Aβ. There was no significant change in the serum catalase activity between the studied groups. Hippocampus catalase activity was reduced in the Aβ group and treatment with ghrelin increased it. The antioxidant capacity of the hippocampus and serum increased in the ghrelin-receiving control group. The hippocampus antioxidant capacity level decreased in the Aβ group, and treatment with ghrelin increased it, but there were no significant changes in the serum antioxidant capacity of animals receiving Aβ. These results provide evidence that the administration of ghrelin has antioxidant properties and protects against hippocampal lipid peroxidation in a rat model of AD.

Alleviation of cognitive deficits in a rat model of glutamate-induced excitotoxicity, using an N-type voltage-gated calcium channel ligand, extracted from Agelena labyrinthica crude venom

“…However, the hyper-activity of this neurotransmitter can induce neurodegeneration through the hyper-stimulation of the NMDA receptors (Dong et al, 2009;Crews and Masliah, 2010). Therefore, agonists of NMDAR like as NMDA, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid can induce excitotoxicity, according to multiple studies (Jarrard, 2002;Zhang et al, 2014Zhang et al, , 2015Hosseini-Sharifabad et al, 2021;Naseri et al, 2022). In addition, NMDA has been used for the induction of cognitive impairment, learning, and memory defects.…”

“…Neurodegeneration in hippocampus area can cause amnesia, forgetfulness, and cognitive impairment, which ends in AD (Crews and Masliah, 2010). AD has the highest prevalence among the neurodegenerative disorders (Naseri et al, 2022;Sarlaki et al, 2022).…”

Ohwia caudata aqueous extract attenuates senescence in aging adipose-derived mesenchymal stem cells

“…Statistical analysis was conducted using GraphPad Prism 9 statistical software (San Diego, CA, USA). To assess the statistical significance of multiple experiments, a one-way analysis of variance followed by Tukey's test was employed [ 37 ]. Statistical significance was defined as a p -value less than 0.05.…”

Ohwia caudata aqueous extract attenuates doxorubicin‐induced mitochondrial dysfunction in Wharton's jelly‐derived mesenchymal stem cells

“…Bradford protein assay was used to determine the total protein content of the whole‐cell extracts 28 . The protein (40 μg) was separated using 8%–15% sodium dodecyl sulfate‐polyacrylamide gels and transferred to a polyvinylidene difluoride membrane (GE, Amersham, UK).…”

“…Bradford protein assay was used to determine the total protein content of the whole-cell extracts. 28 The protein (40 μg) was separated using 8%-15% sodium dodecyl sulfate-polyacrylamide gels and transferred to a polyvinylidene difluoride membrane (GE, Amersham, UK). The membrane was blocked with 5% non-fat milk for 1 h and probed overnight with primary antibodies at 4 C. Protein signals were evaluated using horseradish peroxidase-conjugated secondary antibodies (1:10000) (GE Healthcare, Amersham, UK) and further detected using the Immobilon Western Chemiluminescent HRP substrate (Millipore, Billerica, MA, USA).…”