Abstract

Objective: Autism is a neurodevelopment related disorder with a range of clinical presentations attending serious behavioral and neurological disorders among young children that now occur at epidemic rates in developing countries, India included. The objective of this research was to study the effect of epigallocatechin gallate (EGCG) on sodium valproate-induced autism rats.Methods: On the 12th day of gestation wistar rats were administered with a single intraperitoneal injection of sodium valproate (VPA) (600 mg/kg body weight), which induced autism. The rats were treated with EGCG in varying doses 1, 2 and 5 mg/kg body weight via oral administration. The neuroprotectivity effect of the EGCG was followed by assessing the neurotransmitters and neurobiochemical activities such as serotonin, glutamate and nitrite levels in hippocampus and cerebellum region of the brain. Results: Early prenatal exposure to VPA provokes autistic symptoms. Induction of autism significantly impinged the neurotransmitters and neurochemicals such as serotonin, glutamate and nitrite levels in the brain (hippocampus and cerebellum) increased significantly in the rats exposed to VPA. After treatment with an effective dose of EGCG 2 mg/kg body weight the neurotransmitters and neurochemicals levels were decreased when compared with control and VPA-exposed rats. Conclusion: EGCG ameliorates and reverses autistic attributes possibly due to its neuroprotective activity which could pave the way for future investigation for the possible therapeutic approach.

Highlights

  • Autism is a devastating neurodevelopmental disorder in modern days with core symptoms of impaired social interactions, deficits in verbal and non-verbal communication, and sometimes self-injurious behaviors [1]

  • We report on the effect of epigallocatechin gallate (EGCG) on VPA-induced neurobiochemical alterations in autistic rats

  • VPA exposure induces neurobiochemical alterations such as an increase in serotonin (5-HT) levels in both hippocampus and cerebellum abnormalities when compared with control rats on PND 90, these alternations have been considered to support the validity of the rat model of autism, because serotonin is the key neurotransmitter for autism induction

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Summary

Introduction

Autism is a devastating neurodevelopmental disorder in modern days with core symptoms of impaired social interactions, deficits in verbal and non-verbal communication, and sometimes self-injurious behaviors [1] It is increasing rapidly in India in the ratio of 1:88 children due to increased exposure of environmental insults such as thalidomide, ethanol, and valproic acid due to increased stress during critical periods of neuronal development especially among genetically predisposed children [2]. Serotonergic neurones innervate virtually all parts of the central nervous system, but, like all monoamines, are most concentrated in the brainstem It is responsible for regulating learning, memory, sensory perception, noise sensitivity, behaviour, sleep and appetite [5,6,7]. It is a key brain chemical, identified in the physiological abnormalities in autism spectrum disorders (ASD)

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