Abstract
This study aimed to investigate the protective effects of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS) against ethanol-induced hepatotoxicity and nephrotoxicity in experimental rats. The study involved an intact control group, LPS-RS group, two groups were given ethanol (3 and 5 g/kg/day) for 28 days, and two other groups (LPS-RS + 3 g/kg ethanol) and (LPS-RS + 5 g/kg ethanol) received a daily dose of LPS-RS (800 μg/kg) before ethanol. Ethanol significantly increased the expression of nuclear factor kappa B (NF-κB) and levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the liver tissue and decreased anti-oxidant enzymes. Hepcidin expression was downregulated in the liver, with increased serum levels of ferritin and iron. Prior-administration of LPS-RS alleviated the increase in oxidative stress and inflammatory markers, and preserved iron homeostasis markers. In the kidney, administration of ethanol caused significant increase in the expression of NF-κB and the levels of TNF-α and kidney injury markers; whereas LPS-RS + ethanol groups had significantly lower levels of those parameters. In conclusion; this study reports anti-oxidant, anti-inflammatory and iron homeostasis regulatory effects of the toll-like receptor 4 (TLR4) antagonist LPS-RS against ethanol induced toxicity in both the liver and the kidney of experimental rats.
Highlights
Alcoholic liver disease (ALD) is a worldwide health problem which may result in the development of hepatitis, fatty liver steatosis and cirrhosis [1]
Administration of either 3 g/kg or 5 g/kg of ethanol led to a significant increase in the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) compared to the intact control group
Serum creatinine and blood urea nitrogen (BUN) levels were significantly raised in both ethanol (3 g/kg and 5 g/kg) groups compared to the intact control group
Summary
Alcoholic liver disease (ALD) is a worldwide health problem which may result in the development of hepatitis, fatty liver steatosis and cirrhosis [1]. The damage caused by ethanol is mainly attributed to its metabolic process that results in generation of acetaldehyde and reactive oxygen species (ROS) such as hydrogen peroxide, free hydroxyl radical, and superoxide. These metabolites cause depletion of reduced glutathione (GSH), peroxidation of cellular membranes, oxidation of macromolecules, and eventually lead to progressive injury of hepatocytes [3,4,5]. Agents with anti-inflammatory and anti-oxidative properties might be potential candidates for protection against alcohol-induced liver disease [7,8]
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