Dr. Ahmed M. Kabel

Conference 2024 Live Talk

Talk Title

Baicalin mitigates the neurochemical and the behavioral alterations in valproic acid-induced autism

Authors and Affiliations

Ahmed M. Kabel1,2, Omnia S. El-Deeb3, Amira K. Eltokhy3, Heba M. Arakeep4, Dina A. Ali5, Sanad S. Elkholy6, Rasha O. Elesawy2

1. National Drug Committee, Academy of Scientific Research and Technology, Cairo, Egypt
2. Pharmacology Department, Faculty of Medicine, Tanta University, Tanta, Egypt
3. Medical Biochemistry Department, Faculty of Medicine, Tanta University, Tanta, Egypt
4. Anatomy and Embryology Department, Faculty of Medicine, Tanta University, Tanta, Egypt
5. Clinical Pathology Department, Faculty of Medicine, Tanta University, Tanta, Egypt
6. Physiology Department, Faculty of Medicine, Kafrelsheikh University, Kafr Elsheikh, Egypt

Abstract

Background

Autism is a neuropsychiatric disorder characterized by impairment of social communication together with repetitive or stereotyped behavior. Although its exact etiology isn`t yet completely understood, genetic and environmental factors were thought to participate, to a great extent, in the development of this disorder. Baicalin is a flavonoid of high biomedical value that was recently proven to have numerous pharmacological activities in various pathological disorders. The aim of this study was to investigate the possible effects of baicalin in a rodent model of valproic acid (VPA)-induced autism regarding its potential mitochondrial modulatory, antioxidant, and antiapoptotic effects.

Methods

The current work was carried out using a rodent model of autism by exposing rat fetuses to VPA on the 12.5th day of gestation. Ten male Wistar rats that were born from control pregnant females were considered as group I (control group). Twenty male Wistar rats that were born from prenatal VPA- treated females were further subdivided into two groups: Group II (VPA- induced ASD) and group III (VPA + Baicalin).

Results

Postnatal baicalin improved the postnatal growth, maturation, and motor development. In addition, it ameliorated the repetitive behavior as well as the social deficits in prenatally exposed VPA rats. Moreover, baicalin enhanced the neuronal mitochondrial functions, elevated sirtuin-1 levels in VPA rats’ brain tissues, and restored the antioxidant defense mechanisms to approximate the control values. Moreover, it mitigated the neuronal histopathological and immunohistochemical changes in the brain tissues.

Conclusions

In conclusion, baicalin might provide a promising therapeutic modality for management of autism, possibly via restoration of the mitochondrial functions, augmentation of the antioxidant defenses, and anti-apoptotic effects.