Mousa, H., Morsi, A., Shawky, L. (2022). The possible hepatoprotection promoted by melatonin and alpha-tocopherol in acrylamide-induced liver injury in male albino rats: a histological and immunohistochemical study. Egyptian Journal of Histology, (), -. doi: 10.21608/ejh.2022.173654.1807
Hend R Mousa; Ahmed A. Morsi; Lamiaa M. Shawky. "The possible hepatoprotection promoted by melatonin and alpha-tocopherol in acrylamide-induced liver injury in male albino rats: a histological and immunohistochemical study". Egyptian Journal of Histology, , , 2022, -. doi: 10.21608/ejh.2022.173654.1807
Mousa, H., Morsi, A., Shawky, L. (2022). 'The possible hepatoprotection promoted by melatonin and alpha-tocopherol in acrylamide-induced liver injury in male albino rats: a histological and immunohistochemical study', Egyptian Journal of Histology, (), pp. -. doi: 10.21608/ejh.2022.173654.1807
Mousa, H., Morsi, A., Shawky, L. The possible hepatoprotection promoted by melatonin and alpha-tocopherol in acrylamide-induced liver injury in male albino rats: a histological and immunohistochemical study. Egyptian Journal of Histology, 2022; (): -. doi: 10.21608/ejh.2022.173654.1807
The possible hepatoprotection promoted by melatonin and alpha-tocopherol in acrylamide-induced liver injury in male albino rats: a histological and immunohistochemical study
Articles in Press, Accepted Manuscript, Available Online from 25 November 2022
1Anatomy and Emberyology department, faculty of medicine,Benha university
2Histology and Cell Biology Department, Faculty of Medicine, Fayoum University
3Histology and Cell Biology Department, Faculty of Medicine, Benha University, Benha, Egypt
Abstract
Background: Acrylamide (ACR) is commonly polluting the nearby environment as it forms during the high-temperature food cooking conditions. Several previous studies have confirmed its toxic potential on different body organs. Aim: The current study aims to investigate the possible hepatoprotection elicited by vitamin E (vit E), α-tocopherol versus melatonin (MT) in a rat model of ACR-induced liver toxicity. The putative mechanisms involved in such protection was also examined using histological and immunohistochemical studies. Material and methods: Forty-nine male Wistar albino rats were housed in seven equal groups; control, vit E alone (100 mg/kg/d), MT alone (10 mg/kg/d), ACR-exposed (5 mg/kg/day), ACR/vit E-treated, ACR/MT-treated, and ACR/vit E/MT-treated groups. All treatments were given daily via oral gavage for 8 weeks. In the end of the study, blood samples were collected for measurement of the liver enzymes. Liver lobes were collected for preparation of the tissue homogenates to measure the hepatic concentrations of the oxidative/antioxidative markers. Also, liver samples were prepared for paraffin microtechniques and stained by Hematoxylin & Eosin (H & E) and Masson trichrome staining. Immunohistochemical assays for detection of Bax, Bcl2, and iNOS immunoexpression were performed. Results: ACR-exposed rats showed marked disruption of the biochemical assays, in addition to the hepatocyte disorganization and vacuolar degenerative changes observed in the H & E findings associated with fibrotic tendency in the Masson-stained sections and the disturbed immunoexpressed proteins. Either vit E and/or MT treatment improved the histological and biochemical parameters with normalization in the combined therapy group. Conclusion: Vit E and or MT protected against ACR-mediated liver toxicity by reestablishment of the oxidant/antioxidant balance, downregulation of pro-apoptotic proteins, upregulation of anti-apoptotic proteins, and suppression of the inflammatory pathways. Both combined had synergistic action.