Neuroprotective Impact of Baicalein on Scopolamine Induced Cognitive Deficits Targeting PI3K/Akt /NF-kB pathway

Document Type : Original Article

Authors

1 Physiology Department, Faculty of Medicine, Menoufia University, Egypt

2 Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Menoufia University, Egypt

3 Pharmacology Department, Faculty of Medicine, Suez Canal University, Egypt

4 Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Egypt

5 Clinical Pharmacology Department, Faculty of medicine, Menoufia University

6 Medical Physiology Department, Faculty of Medicine, Menoufia University, Egypt Medical Physiology Department, Faculty of Medicine, King Abdulaziz University, KSA

7 Internal Medicine Department Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.

8 Histology and Cell Biology, Faculty of Medicine, Assiut University Histology, Faculty of Medicine, Aqaba Medical Sciences University

9 Psychiatry Department, Faculty of Medicine, Menoufia University, Egypt

10 Zoology Department - Faculty of Science, Menoufia University, Egypt

11 Forensic Medicine and Clinical Toxicology, Department, Faculty of Medicine, Menoufia University, Egypt

12 Clinical Pathology Department, National Liver Institute, Menoufia University, Egypt

13 Medical Physiology Department, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt

Abstract

Dementia is a substantial public health concern. Scopolamine (Scop) is a muscarinic acetylcholine receptor antagonist that induces cognitive impairment. The objective of this study was to demonstrate the potential mechanisms by which Baicalein (Baic) might protect against cognitive abnormalities caused by Scop. The thirty male albino rats were divided into three groups: Scop, Scop plus Baic, and control (10/group). After four weeks neurobehavioral assessment was conducted in conjunction with the measurement of hippocampal MDA, SOD, acetylcholine, BDNF, TNF-α, IL-6, IL-1β, and PI3K, Akt, and NF-kB gene expression. The immunohistochemical analysis of Bax, Tau, and GFAP markers was assessed. Scop induced cognitive impairment in rats with a significant increase in the expression of MDA, TNF-α, IL-6, IL-1β, and NF-kB genes, as well as a substantial decrease in the expression of hippocampal SOD, BDNF, acetylcholine, and hippocampal PI3K and Akt genes, as well as an upregulation of GFAP, Tau, and Bax immunoreactions, however Baic dramatically improved Scop-induced cognitive impairment. We can conclude that Baic induced anti-oxidant, anti-inflammatory, neurotrophic, and anti-apoptotic mechanisms in addition to modifying the PI3K/Akt/NF-kB signaling cascade to mitigate the cognitive impairments brought on by Scop.

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