Author(s): P. Kumaravel, G. Melchias, N. Vasanth, T. Manivasagam

Email(s): kumaravelbiotech@gmail.com

DOI: 10.5958/0974-360X.2017.00260.8   

Address: P. Kumaravel1*, G. Melchias2, N. Vasanth2, T. Manivasagam3
1Department of Biotechnology, St. Joseph’s College (Autonomous), Tiruchirappalli, Tamil Nadu, India.
2Department of Botany, St. Joseph’s College (Autonomous), Tiruchirappalli, Tamil Nadu, India.
3Department of Biochemistry and Biotechnology, Annamalai University, Chidambaram, Tamil Nadu, India.
*Corresponding Author

Published In:   Volume - 10,      Issue - 5,     Year - 2017


ABSTRACT:
Pregnant rats were administered by either sodium valproate (VPA) with 250 mg/kg during fetal neural tube development on embryonic day 12, induces neural tube defects and impairment in behaviors related to autistic spectrum disorder in newborns, which make it a useful animal model of autism. Male rat pups were subjected to behavioral testing to assess exploratory activity, peripheral and central movements and motor activity like grooming and rearing on postnatal day 90. We investigated the role of EGCG (2mg/kg) in reversing cardinal behavioral changes induced by VPA exposed rats. Consumption of EGCG has been associated with neuronal protection against the impact of toxicants. EGCG exerts neuronal cytoprotective action possibly due to anti-oxidant action and neuroprotective effect could be efficacious in the management of autism.


Cite this article:
P. Kumaravel, G. Melchias, N. Vasanth, T. Manivasagam. Epigallocatechin Gallate Attenuates Behavioral Defects in Sodium Valproate Induced Autism Rat Model. Research J. Pharm. and Tech. 2017; 10(5): 1477-1480. doi: 10.5958/0974-360X.2017.00260.8

Cite(Electronic):
P. Kumaravel, G. Melchias, N. Vasanth, T. Manivasagam. Epigallocatechin Gallate Attenuates Behavioral Defects in Sodium Valproate Induced Autism Rat Model. Research J. Pharm. and Tech. 2017; 10(5): 1477-1480. doi: 10.5958/0974-360X.2017.00260.8   Available on: https://rjptonline.org/AbstractView.aspx?PID=2017-10-5-35


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RNI: CHHENG00387/33/1/2008-TC                     
DOI: 10.5958/0974-360X 

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