Abstract
The aim of this study was to determine the malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in colchicine induced Alzheimer’s disease (AD), resveratrol (RS) treated and RS + donepezil (DPZ) treated rat models. The objective was to compare the MDA level and SOD activity among these rat models. The present study included 3 months old male albino Wistar rats, which were in-house bred and weighting about 220–250 g. The rats were divided into nine subgroups which included control, sham, AD induced, RS treated and DPZ treated groups in different doses and combinations. The lipid peroxidation product for MDA in the brain homogenate was measured by estimating the levels of thiobarbituric acid reactive substance. Estimation of SOD was done by the method of autoxidation of pyrogallol by Marklund and Marklund. There was a marked increase in the MDA levels in AD induced group in comparison to the control group (p < 0.05). The SOD activity was higher in the RS 10 and RS 20 treated groups in contrast to the AD group (p < 0.05). In DPZ + RS group, there was a substantial increase in the SOD activity (p < 0.05). It is also observed that the RS 20 treatment group showed higher SOD activity than the RS 10 group (p < 0.05). This study showed that, AD induced group had elevated levels of MDA, which indicates the poor oxidative stress–defence mechanism. The RS 10 and RS 20 groups showed higher SOD activity in comparison to the AD group, which indicated the improved oxidative stress–defence mechanism. The RS + DPZ group showed higher SOD activity, indicating a synergistic effect of DPZ and RS.
Highlights
Alzheimer’s disease (AD) is an irreversible, progressive brain disorder which is often associated with the other human diseases (Surguchov 2020)
The comparison of MDA levels and superoxide dismutase (SOD) activity among different subgroups were compared each other and the ‘p’ values are given in Tables 2 and 3
Our study has proved that, when RS was administered with the combination of DPZ, the antioxidant activity of the brain will be more effectual, which can prevent the neuro apoptosis
Summary
Alzheimer’s disease (AD) is an irreversible, progressive brain disorder which is often associated with the other human diseases (Surguchov 2020). The neuronal degeneration in this disorder is characterized by the cognitive dysfunction, leading into dementia (Enna and Coyle 1998). The oxidative stress was reported to be among the aetiological factors of AD (Tonnies et al 2017). The pathophysiology involved in AD is the intra-neuronal accumulation of hyperphosphorylated tau protein in the form of neurofibrillary tangles and extra cellular deposition of the beta amyloid plaques due to the oxidative stress (Huang et al 2016). Brain is the most susceptible organ for oxidative stress due to its high oxygen consumption (Gomes et al 2018). The reactiveoxygen species (ROS) are highly produced in the brain of AD patients due to the stress, which leads to the oxidative
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