"Comparative evaluation of different chemical agents induced Autism Spectrum Disorder in experimental Wistar rats".


Journal

Behavioural brain research
ISSN: 1872-7549
Titre abrégé: Behav Brain Res
Pays: Netherlands
ID NLM: 8004872

Informations de publication

Date de publication:
26 Feb 2024
Historique:
received: 30 07 2023
revised: 04 10 2023
accepted: 18 10 2023
medline: 29 11 2023
pubmed: 6 11 2023
entrez: 3 11 2023
Statut: ppublish

Résumé

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition with uncertain etiology and pathophysiology. Several studies revealed that the commonly used animal models like Valproic Acid (VPA) and Propionic Acid (PPA) do not precisely represent the disease as the human patient does. The current study was conducted on different chemically (VPA, PPA, Poly I:C, Dioxin (2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)) & Chlorpyrifos (CPF)) induced ASD-like animal models and validated the best suitable experimental animal model, which would closely resemble with clinical features of the ASD. This validated model might help to explore the pathophysiology of ASD. This study included rat pups prenatally exposed to VPA, PPA, Poly I:C, Dioxin & CPF within GD9 to GD15 doses. The model groups were validated through developmental and behavioral parameters, Gene Expressions, Oxidative Stress, and Pro-inflammatory and Anti-inflammatory cytokines levels. Developmental and neurobehavioral parameters showed significant changes in model groups compared to the control. In oxidative stress parameters and neuro-inflammatory cytokines levels, model groups exhibited high oxidative stress and neuro-inflammation compared to control groups. Gene expression profile of ASD-related genes showed significant downregulation in model groups compared to the control group. Moreover, the Poly I:C group showed more significant results than other model groups. The comparison of available ASD-like experimental animal models showed that the Poly I:C induced model represented the exact pathophysiology of ASD as the human patient does. Poly I:C was reported in the maternal immune system activation via the inflammatory cytokines pathway, altering embryonic development and causing ASD in neonates.

Identifiants

pubmed: 37923221
pii: S0166-4328(23)00446-1
doi: 10.1016/j.bbr.2023.114728
pii:
doi:

Substances chimiques

Dioxins 0
Valproic Acid 614OI1Z5WI
Cytokines 0
Chlorpyrifos JCS58I644W
Poly I 25249-22-3

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

114728

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Amit Raj Sharma (AR)

Department of Neurology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Gitika Batra (G)

Department of Neurology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Neha Dhir (N)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Ashish Jain (A)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Tanish Modi (T)

Clinical Trainee, Department of Neurology, PGIMER, Chandigarh, India.

Lokesh Saini (L)

All India Institute of Medical Sciences, Paediatric Neurology, Jodhpur, India.

Neetika Thakur (N)

Department of Endocrinology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Abhishek Mishra (A)

University of Minnesota Twin Cities, Department of Biomedical Sciences, USA.

Rahul Solomon Singh (RS)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Ashutosh Singh (A)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Rubal Singla (R)

University of Minnesota Twin Cities, Department of Biomedical Sciences, USA.

Ajay Prakash (A)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Manoj Goyal (M)

Department of Neurology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Alka Bhatia (A)

Department of Experimental Medicine and Biotechnology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Bikash Medhi (B)

Department of Pharmacology, Post Graduate Institute Medical Education and Research, Chandigarh, India.

Manish Modi (M)

Department of Neurology, Post Graduate Institute Medical Education and Research, Chandigarh, India. Electronic address: modipgi@gmail.com.

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Classifications MeSH