Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation.

Autor: Abo-Zaid OA; Biochemistry and Molecular Biology Department, Faculty of Vet. Med, Benha University, Moshtohor, Banha, Egypt., Moawed FS; Health Radiation Research, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt. fatmasearch5@yahoo.com.; Egyptian Atomic Energy Authority, Nasr City, Cairo, 11787, Egypt. fatmasearch5@yahoo.com., Taha EF; Health Radiation Research, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt., Ahmed ESA; Radiation Biology Research, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt., Kawara RS; Biochemistry and Molecular Biology Department, Faculty of Vet. Med, Benha University, Moshtohor, Banha, Egypt.
Jazyk: angličtina
Zdroj: Cell stress & chaperones [Cell Stress Chaperones] 2023 Nov; Vol. 28 (6), pp. 709-720. Date of Electronic Publication: 2023 Jun 27.
DOI: 10.1007/s12192-023-01363-8
Abstrakt: The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction and/or exposure to IR resulted in a significant decrease in the serum levels of T3 and T4 associated with increased levels of lipid peroxidation end product, malondialdehyde (MDA), and nitrites (NO) in the brain tissue homogenate. Also, hypothyroidism and /or exposure to IR markedly enhance the endoplasmic reticulum stress by upregulating the gene expressions of the protein kinase RNA-like endoplasmic reticulum kinase (PERK), activated transcription factor 6 (ATF6), endoplasmic reticulum-associated degradation (ERAD), and CCAAT/enhancer-binding protein homologous protein (CHOP) in the brain tissue homogenate associated with a proapoptotic state which indicated by the overexpression of Bax, BCl2, and caspase-12 that culminates in brain damage. Meanwhile, the PTU and /or IR-exposed rats treated with MEE reduced oxidative stress and ERAD through ATF6. Also, the MEE treatment prevented the Bax and caspase-12 gene expression from increasing. This treatment in hypothyroid animals was associated with neuronal protection as indicated by the downregulation in the gene expressions of the microtubule-associated protein tau (MAPT) and amyloid precursor protein (APP) in the brain tissue. Furthermore, the administration of MEE ameliorates the histological structure of brain tissue. In conclusion, MEE might prevent hypothyroidism-induced brain damage associated with oxidative stress and endoplasmic reticulum stress.
(© 2023. The Author(s).)
Databáze: MEDLINE
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