Cilostazol attenuated prenatal valproic acid-induced behavioural and biochemical deficits in a rat model of autism spectrum disorder

Autism spectrum disorder (ASD) is categorized as a neurodevelopmental disorder, presenting with a variety of aetiological and phenotypical features. Inhibiting the enzyme phosphodiesterase-3 (PDE3) with cilostazol is known to produce beneficial effects in several brain disorders. The pharmacological...

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Published in:	Journal of pharmacy and pharmacology 2021-10, Vol.73 (11), p.1460-1469
Main Authors:	Luhach, Kanishk, Kulkarni, Giriraj T, Singh, Vijay P, Sharma, Bhupesh
Format:	Article
Language:	eng
Subjects:	Animals Anticonvulsants - adverse effects Anxiety - prevention & control Autism Spectrum Disorder - chemically induced Autism Spectrum Disorder - drug therapy Behavior, Animal - drug effects Biomarkers - metabolism Brain - drug effects Brain - metabolism Cilostazol - pharmacology Cilostazol - therapeutic use Disease Models, Animal Female Inflammation - metabolism Inflammation - prevention & control Locomotion - drug effects Male Maze Learning Motor Activity - drug effects Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Oxidative Stress - drug effects Pregnancy Prenatal Exposure Delayed Effects - drug therapy Rats Rats, Wistar Social Behavior Valproic Acid - adverse effects
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Summary:	Autism spectrum disorder (ASD) is categorized as a neurodevelopmental disorder, presenting with a variety of aetiological and phenotypical features. Inhibiting the enzyme phosphodiesterase-3 (PDE3) with cilostazol is known to produce beneficial effects in several brain disorders. The pharmacological outcome of cilostazol administration was investigated in prenatal valproic acid (VPA)-induced ASD deficits in albino Wistar rats. Cilostazol was administered in two doses (30/60 mg/kg) to male rats born of females administered with VPA on gestational day 12. Behavioural assays on locomotion (open field), social interaction, repetitive behaviour (y-maze) and anxiety (elevated plus maze) were performed in all groups. Further, biochemical assessments of markers associated with neuronal function (BDNF, pCREB), inflammation (TNF-α, IL-6, IL-10) and oxidative stress were carried out in frontal cortex, hippocampus, striatum and cerebellum. The cilostazol regimen, attenuated prenatal VPA exposure associated hyperlocomotion, social interaction deficits, repetitive behavior, and anxiety. Further, biochemical markers such as BDNF, pCREB, IL-10 and GSH were found to be significantly increased contrary to markers such as TNF-α, IL-6 and TBARS in the assessed brain regions. Cilostazol rectified core behavioural traits while producing significant changes to biochemistry in the brain, suggesting benefits of cilostazol administration in experimental models of ASD.
ISSN:	0022-3573 2042-7158