Baicalein mitigates cognitive impairment in chronic stress rat model by downregulating TLR4/NF-kB signaling pathway

Document Type : Original Article

Authors

1 Medical Physiology Department, Faculty of medicine, Suez Canal University Ismailia, Egypt

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 Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt, Department of Anatomy and Histology, College of Medicine, Qassim University, Buraydah, Saudi Arabia

5 Clinical Pharmacology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt

6 Department of Medical Biochemistry & Molecular biology , Faculty of Medicine, Benha University

7 Pathology Department, Faculty of medicine Mansoura University, Egypt

8 Zoology Department - Faculty of Science, Menoufia University, Menoufia, Egypt.

9 Medical Physiology Department, Faculty of Medicine, Cairo University, Cairo, Egypt

10 Department of Psychiatry and Neurology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt

11 Internal Medicine and Nephrology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt

Abstract

Introduction: Chronic stress can significantly impair memory and learning processes by changing the hippocampus and other brain regions. Baicalein (Baic) has been shown to possess anti-inflammatory and antioxidant qualities.
Objective: to demonstrate the neuroprotective mechanism of Baic in stress-induced cognitive impairments.
Material & methods: Thirty male Wister albino rats were split into three: control, stress, and stress + bait. Rats underwent NOR and EPM tests, hippocampus gene expression of TLR4, NF-kB, and BDNF was evaluated, and serum corticosterone, hippocampal MDA, SOD, TNF-α, and IL-6 were examined. TLR4 and NF-kB immunoreaction for hippocampus were performed.
Results: In contrast to the control group, which had higher hippocampal TLR4 and NF-kB immunoreaction and a significantly lower discrimination index of the NOR test, time in the open arms of EPM, SOD, and gene expression of BDNF, stress demonstrated cognitive impairment by significantly increasing serum corticosterone, hippocampal MDA, TNF-α, IL-6, and hippocampal gene expression of TLR4 and NF-kB. Baic significantly improved the alterations in the brain caused by stress.
Conclusion: Baic reduced stress-induced cognitive deficits by down-regulation of the TLR4/NF-kB signaling pathway as well as neurotrophic, antioxidant, and anti-inflammatory mechanisms.

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