Abstract
Purpose: To investigated the effect of hemin, a heme oxygenase-1 (HO-1) inducer, on nicotinamide adenine dinucleotide phosphate oxidase (NOX) expression in rats with alcohol-induced liver injury. Methods: Male Wistar rats were randomly divided into four groups consisting of the control group, the ethanol (EtOH) group, the EtOH + zinc protoporphyrin IX (ZnPP-IX) group and EtOH + hemin group. Hepatic NOX gene expression and immunohistochemistry of hepatic NOX1 and NOX4 were investigated in week 4. Results: EtOH significantly increased levels of NOX. An immunohistochemical study demonstrated a high number of immunopositive hepatocytes for NOX1 in the EtOH group and EtOH + ZnPP-IX group compared with the control group. Hemin administration downregulated NOX gene expression and lowered the number of immunopositive hepatocytes for NOX1. In contrast, ZnPP-IX (HO-1 inhibitor) administration caused upregulation of NOX gene expression and increased the number of immunopositive hepatocytes for NOX1. Conclusion: HO-1 inducer, hemin, alleviates oxidative stress-induced alcoholic liver injury by reducing NOX, especially NOX1. Keywords: NADPH oxidase, Immunohistochemistry, Heme oxygenase-1, Hemin, Reactive oxygen species, Alcohol-induced liver disease
Highlights
Alcohol-induced liver disease is an increasing global health problem
The rats treated with hemin had statistically significantly reduced (p < 0.001) nicotinamide adenine dinucleotide phosphate oxidase (NOX) mRNA levels compared with rats in the EtOH group and the EtOH + zinc protoporphyrin IX (ZnPP-IX) group
The rats treated with heme oxygenase-1 (HO-1) inducer hemin demonstrated a lower number of immunopositive hepatocytes for NOX1 compared to rats in the
Summary
Alcohol-induced liver disease is an increasing global health problem. Acute alcohol consumption leads to fatty liver. Fatty liver is a reversible injury, its progression can develop into more severe liver problems including steatohepatitis and cirrhosis [1]. Previous studies showed that oxidative stress is an important factor contributing to the development of alcohol-induced liver injury [2]. Ethanol consumption has been shown to increase the production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), decrease cellular antioxidant levels, and eventually enhance oxidative stress in many tissues, especially the liver [3]. ROS/RNS play the critical roles in damage to several macromolecules especially lipids, proteins and DNA, eventually causing alcohol-induced liver disease [4]
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