Document Type : Original Article
Authors
1
Physiology department, faculty of medicine, Suez canal university
2
Medical physiology department, faculty of Medicine, Menoufia University
3
Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
4
Psychiatry Department, Sulaiman Alrajhi University, AL Bukayriyah, Saudi Arabia Psychiatry Department, Faculty of Medicine, Assiut University, Assiut, Egypt.
5
Clinical Pharmacology Department, Faculty of medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
6
Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
7
Pathology Department, Faculty of medicine for Girls, Al-Azhar University
8
Human Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt Department of Anatomy and Histology, College of Medicine, Qassim University, Buraydah, Saudi Arabia
9
Physiology Department, Faculty of Medicine for Girls, Al-Azhar University, Cairo 11884, Egypt
10
Medical Physiology Department , Faculty of Medicine, Ain Shams University, Cairo, Egypt
Abstract
Introduction: A neurodevelopmental disease known as autism spectrum disorder (ASD) is linked to stereotypical behavior and poor social skills. Resveratrol (Res) has been shown to possess anti-inflammatory and antioxidant impacts.
Objective: to demonstrate the underlying mechanisms and neuroprotective impact of Res in VPA-induced ASD
Material & methods: Thirty male Swiss mice were split into three : control, VPA, and VPA+Res. Following neurobehavioral testing, the rats were sacrificed, and the cerebellar gene expression of Nrf2 and HO-1 was evaluated together with the measurements of MDA, SOD, TNF-α, IL-6, IL-10 and serotonin. GFAP and Caspase-3 cerebellar immunoreactions were performed.
Results: While the VPA group's time of central crossing in OFT, percentage of alternation in the T maze test, Cerebellar SOD, Cerebellar IL-10, and Cerebellar gene expression of Nrf2 and HO-1 were dramatically lower than those of the control, the VPA 's number of crossing slots in OFT, rearing frequency in OFT, Cerebellar MDA, Cerebellar TNF-α, and Cerebellar IL-6 were all dramatically higher than those of the control group with impairments in social interaction. Res substantially reduced VPA-induced ASD.
Conclusion: In addition to enhancing gliosis and up-regulating the Nrf2/HO-1 signaling pathway, Res also reduced VPA-induced ASD through anti-oxidant, anti-inflammatory and antiapoptotic pathways.
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