Aims: Oxidative stress and activation of pro-apoptotic mediators have been associated with the pathogenesis of Huntington’s disease. Andrographolide (ANDRO) is a well-known antioxidant and inhibitor of pro-apoptotic mediator, nuclear factor kappa B (NF-kB). Study Design: The present study was hence designed to evaluate the effect of ANDRO in Huntington’s disease. Place and Duration of Study: Department of Pharmacology, Khalsa College of Pharmacy, Amritsar, India between March 2018 and July 2018. Methodology: Five groups (n=6) of Sprague dawley rats were used. Normal group animals were kept untreated. The control group was administered 3-Nitro propionic acid (3-NP) for seven days. The three treament groups received 3-NP followed by ANDRO intraperitoneally for seven days. On 8th day, behavioral and coordination parameters were evaluated using multiple tests. Oxidative stress and anti-oxidant enzyme levels in brain tissue were also evaluated. Brain tissues were also evaluated using Haematoxylin-eosin staining. Results: Administration of 3-NP resulted in motor incoordination and muscle weakness as indicated by behavioral tests. Biochemically, there was an increase in the oxidative stress and depletion of free radical scavenging. Histopathologically, there was severe neuronal degeneration and neural tissue apoptotic changes in the rat striatum. ANDRO administration resulted in significant decrease in the muscle incoordination in the behavioral tests and also decreased prooxidative biochemical changes. Brain tissues of the ANDRO treated animals showed protection against neuronal damage and neurodegeneration. Conclusion: The results indicate that the use of ANDRO may afford protection against Huntington’s disease associated muscle incoordination and subsequent neurodegeneration. Present study provides a lead for further investigation of role of NF-kB inhibitors in Huntington’s disease and possible development of low-cost natural medication.
Background: The present study was designed to evaluate the protective effect of Prunus amagdylus nut kernels against aluminium chloride induced spatial memory deficits in rats.Methods: Plant material was extracted, and extracts were evaluated for anti-oxidants by DPPH method. Animals were divided into four groups of five animals each. Group 1 was normal group and was kept undisturbed. Group 2 was administered with Aluminium Chloride (4.2mg/kg i.p) for 21 successive days. Group 3 and 4 were pre-administered with Prunus amygdalus methanolic extract at dose 0.5 and 1mg/kg/ p.o) one hour prior to aluminium chloride administration. The memory parameters (both acquisition and retrieval) were evaluated using Morris water maze. After behavioural studies, the animals were sacrificed by decapitation and braintissue thiobarbituric acid reactive substances (TBARS), glutathione (GSH) and catalase activity were measured. Brain tissues from all the groups were histopathologically evaluated using Haematoxylin-eosin staining.Results: Administration of Aluminium chloride resulted in severe memory deficits and neurochemical alterations as was indicated by significant increase in Transfer Latency (TL) time on Morris water maze and increase in the brain tissue TBARS levels in the control group animals. There was significant reduction in the GSH and catalase levels indicating decreased anti-oxidant defence. Histopathologically, control group animal brain tissue showed signs of neuroinflammation. All behavioural and neurochemical and histopathological changes were prevented to a significant extent in the animal groups pre-treated with Prunus amygdalus extract.Conclusions: Methanolic extract of Prunus amaygdalus possesses protective activity against aluminium chloride induced neurotoxicity and associated memory deficits.
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