Antioxidant and Iron-Binding Properties of Curcumin, Capsaicin, andS-Allylcysteine Reduce Oxidative Stress in Rat Brain Homogenate

Abstract Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder marked by social and communication deficits as well as repetitive behaviour. Several studies have found that overactivation of the PI3K/AKT/mTOR signalling pathways during brain development plays a significant role in autism pathogenesis. Overexpression of the PI3K/AKT/mTOR signalling pathway causes neurological disorders by increasing cell death, neuroinflammation, and oxidative stress. Chrysophanol, also known as chrysophanic acid, is a naturally occurring chemical obtained from the plant Rheum palmatum. This study aimed to examine the neuroprotective effect of CPH on neurobehavioral, molecular, neurochemical, and gross pathological alterations in ICV-PPA induced experimental model of autism in adult rats. The effects of ICV-PPA on PI3K/AKT/mTOR downregulation in the brain were studied in autism-like rats. Furthermore, we investigated how CPH affected myelin basic protein (MBP) levels in rat brain homogenate and apoptotic biomarkers such as caspase-3, Bax, and Bcl-2 levels in rat brain homogenate and blood plasma samples. Rats were tested for behavioural abnormalities such as neuromuscular dysfunction using an actophotometer, motor coordination using a beam crossing task (BCT), depressive behaviour using a forced swim test (FST), cognitive deficiency, and memory consolidation using a Morris water maze (MWM) task. In PPA-treated rats, prolonged oral CPH administration from day 12 to day 44 of the experimental schedule reduces autistic-like symptoms. Furthermore, in rat brain homogenates, blood plasma, and CSF samples, cellular, molecular, and cell death markers, neuroinflammatory cytokines, neurotransmitter levels, and oxidative stress indicators were investigated. The recent findings imply that CPH also restores abnormal neurochemical levels and may prevent autism-like gross pathological alterations, such as demyelination volume, in the rat brain.

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Herbal snuff (AK-47 and HAM) induce oxidative stress and increase acetylcholinesterase enzyme activity in rat brain

GSC Biological and Pharmaceutical Sciences ◽

10.30574/gscbps.2021.17.3.0355 ◽

2021 ◽

Vol 17 (3) ◽

pp. 171-176

Author(s):

Bawa Yusuf Muhammad ◽

Sulaiman Abdullahi Barau ◽

Moses Zira Zaruwa ◽

Rabo Maikefi

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Rat Brain ◽

Brain Homogenate ◽

Albino Rats ◽

Antioxidant Enzyme Activities ◽

High Concentration ◽

Treatment Groups ◽

Brain Ache Activity ◽

Acetylcholinesterase Enzyme

Snuff has resurfaced not only in western countries but in Africa including Nigeria. It is now almost generally acceptable, among young and old in Nigeria. This research was designed to investigate the Effect of Hajiya Aisha Manpower (HAM) and AK-47 on Antioxidant Status and Acetylcholinesterase enzyme activity (AchE) of Wister Albino Rats. Thirty (30) Wister rats (110-120 g) were arbitrarily divided into five groups. Group1 (control); received only distilled water. Groups 2 and 3 (received 6 mg and 3 mg/kg b.w.t of HAM respectively). Groups 4 and 5 (received 6 mg and 3 mg/kg b.w.t AK-47 of respectively). After two months of treatments, the rats were anesthetized, blood samples were taken through heart puncture and brains of all rats were isolated and homogenized. The Result revealed Non-significant decrease in Superoxide dismutase (SOD), glutathione peroxidase (GPx) activities and concomitant increase in GSH levels in treatment groups were observed in relation to the control. While a substantial increase (p˂ 0.5) in MDA was detected in treatment groups. Brain AchE activity increased significantly in all treatment groups in relation to the control. We conclude that Both AK-47 and HAM at high concentration induce oxidative stress, decreased antioxidant enzyme activities and promote degradation of acetylcholine in rat brain homogenate.

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PI3K/AKT/mTOR Signalling Inhibitor Chrysophanol Ameliorates Neurobehavioural and Neurochemical Defects in Propionic Acid-induced Experimental Model of Autism

10.21203/rs.3.rs-705335/v1 ◽

2021 ◽

Author(s):

Aarti Sharma ◽

Sidharth Mehan

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Blood Plasma ◽

Rat Brain ◽

Forced Swim Test ◽

Brain Homogenate ◽

Autism Spectrum ◽

Pathological Changes ◽

And Oxidative Stress ◽

Mtor Signalling

Abstract Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by social-communication deficits and repetitive behaviour. Several studies have revealed that overactivation of the PI3K/AKT/mTOR signalling pathways during brain development plays an important role in the pathogenesis of autism. The PI3K/AKT/mTOR signalling pathway overexpression produces neurological abnormalities by increasing cell death, neuroinflammation, and oxidative stress. Chrysophanol, also known as chrysophanic acid, is a natural substance derived from the plant Rheum palmatum, a well-known Chinese herbal remedy with potential pharmacological applications. The purpose of this study was to look into the neuroprotective effect of CPH on neurobehavioral, molecular, neurochemical, and gross pathological changes in ICV-PPA-induced autism-like rats, with a particular emphasis on its effect on PI3K/AKT/mTOR downregulation in the brain. Furthermore, we looked at how CPH affected the levels of myelin basic protein (MBP) in rat brain homogenate, as well as apoptotic markers such caspase-3, Bax, and Bcl-2 levels in rat brain homogenate and blood plasma samples. Rats were examined for behavioural abnormalities, like neuromuscular dysfunction using actophotometer, motor coordination by beam crossing task (BCT), depressive behaviour with forced swim test (FST), cognitive deficit, and consolidation of memory using Morris water maze (MWM) task. Prolonged oral CPH administration from day 12 to day 44 of the experimental schedule reduces autistic-like symptoms in PPA-treated rats. In addition, cellular, molecular, cell death markers, neuroinflammatory cytokines, neurotransmitter levels, and oxidative stress indicators have been examined in rat brain homogenates, blood plasma, and CSF samples. The current findings suggest that CPH also restores the altered neurochemical levels and potentially prevents autism-like gross pathological changes, including demyelination volume in the rat brain.

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