
Vitamin E and Lactobacillus Provide Protective Effects Against Liver Injury Induced by HgCl2: Role of CHOP, GPR87, and mTOR Proteins
Author(s) -
Ahlam M. Alhusaini,
Shahad Alghilani,
Waad N. Alhuqbani,
Iman H. Hasan
Publication year - 2021
Publication title -
dose-response
Language(s) - English
Resource type - Journals
ISSN - 1559-3258
DOI - 10.1177/15593258211011360
Subject(s) - oxidative stress , chemistry , toxicity , glutathione , liver injury , pharmacology , vitamin e , chop , medicine , apoptosis , endocrinology , biochemistry , antioxidant , enzyme
Background and Objective: Mercury is one of the most harmful heavy metals and its toxicity causes severe multi-organ dysfunction. This study was designed to explore novel molecular pathways involved in the hepatoprotective effect of vitamin E (Vit-E) and Lactobacillius plantarum (Lac-B) against mercury toxicity.[Formula: see text]Method: Acute hepatotoxicity was induced by administration of high dose of mercuric chloride (HgCl 2 ) in male rats, Vit-E or/and Lac-B were given along with HgCl 2 for 2 weeks. The effects of those antioxidants were studied focusing on their anti-apoptotic, anti-oxidative stress and anti-inflammatory eficacies. Histopathological examinations were also conducted.Results: The administration of HgCl 2 induced liver injury which manifested by elevation in serum ALT and AST. Liver MDA, caspase-3 and TNF-α levels were markedly increased; whereas, GSH level and SOD activity were declined. HgCl 2 significantly elevated the expressions of hepatic CHOP, GPR87, NF-κB and mTOR. Histopathological examination revealed massive hepatocyte degeneration following HgCl 2 administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved hepatic architecture.Conclusion: Vit-E and Lac-B provided protective effect against HgCl 2 -induced hepatotoxicity via reduction of oxidative stress and inflammation, and downregulation of CHOP, GPR87, NF-κB and mTOR proteins’ expressions.