Browsing by Author "Mehanna, Eman T"

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Alcohol-Induced Hepatic Fibrosis and the Relation between Hepcidin and Liver Fibrosis
(Suez Canal University, 2024-05) Ali, Al-shimaa A; Aborehab, Nora M; Saleh, Samy M; Mehanna, Eman T
Abstract: Alcoholic liver disease (ALD) is a worldwide health problem that may lead to development of fatty liver steatosis, hepatitis and cirrhosis. Alcohol is known to exert a harmful effect on a variety of human tissues. In particular, the liver is the major site of alcohol-induced damage because it is the direct recipient of the blood that contains elevated levels of alcohol, and it is the major organ responsible for alcohol metabolism. The damage caused by ethanol is mainly attributed to its metabolic process that results in production of acetaldehyde and reactive oxygen species (ROS) such as hydrogen peroxide, superoxide and free hydroxyl radical. These metabolites cause depletion of reduced glutathione (GSH), peroxidation of cellular membranes, oxidation of macro-molecules such as proteins and nucleic acids, and eventually lead to progressive injury of hepatocytes. Additionally, ethanol and its metabolic products enhance the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The enhanced production of those inflammation factors; stimulated partially by oxidative stress; results in cytokine imbalance and immune disorders, leading to further hepatic damage. Thus, agents with anti-inflammatory and anti-oxidative properties might be potential candidates for protection against alcohol-induced liver disease. The metabolic functions of the alcoholic liver are seriously affected. Disorders in iron metabolism are characteristic of ALD. Abnormal levels of iron, ferritin, and transferrin were reported in ALD. Hepcidin, the principle hepatic regulator of the metabolism of iron, is decreased in ALD.
Anti-Oxidant and Anti-Inflammatory Effects of Lipopolysaccharide from Rhodobacter sphaeroides against Ethanol-Induced Liver and Kidney Toxicity in Experimental Rats
(MDPI, 08/12/2021) Mehanna, Eman T; Ali, Al-Shimaa A; El-Shaarawy, Fatma; Mesbah, Noha M; Abo-Elmatty, Dina M; Aborehab, Nora M
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.