title: Heme oxygenase-1 alleviates alcoholic liver steatosis: histopathological study.
abstract: Excessive alcohol consumption is one of the most important causes of hepatic steatosis, which involves oxidative stress. In particular, increased oxidative stress has been strongly linked to stimulation of the expression of heme oxygenase-1 (HO-1). This study aimed to investigate whether HO-1 could alleviates alcoholic steatosis in rats. Male Wistar rats were randomly divided into 4 groups: 1) the control group, 2) the EtOH group, 3) the EtOH + ZnPP-IX group and 4) the EtOH + Hemin group. Liver histopathology was investigated in weeks 1 and 4 after the start of the treatment period. Alcohol treatment significantly increased the hepatic malondialdehyde (MDA) levels, an oxidative stress marker. In addition, it increased the triglyceride, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in both weeks. Gross examination demonstrated a yellowish and slightly enlarged liver in the alcohol-treated rats. Hematoxylin and eosin (H&E) and Oil Red O staining indicated hepatic steatosis, which was characterized by diffuse, extensive fatty accumulation and discrete lipid droplets of variable size in hepatocytes of the alcohol-treated rats. Administration of the HO-1 inducer hemin resulted in upregulation of hepatic HO-1 gene expression, reduced the MDA, triglyceride, ALT and AST levels and alleviated alcoholic hepatic steatosis, whereas administration of the HO-1 inhibitor zinc protoporphyrin IX (ZnPP-IX) resulted in downregulation of hepatic HO-1 gene expression and could not alleviate alcoholic hepatic steatosis either week. In conclusion, HO-1 could alleviate alcoholic hepatic steatosis in male Wistar rats and may be useful in development of a new therapeutic approach.
authors.affiliation: School of Medicine, Walailak University, Nakhon Si Thammarat 80161, Thailand; The Pathobiology of the Cell and Tissue Research Group, Walailak University, Nakhon Si Thammarat 80161, Thailand.
authors.forename: Sarawoot
authors.initials: S
authors.lastname: Palipoch
authors.affiliation: School of Medicine, Walailak University, Nakhon Si Thammarat 80161, Thailand; The Pathobiology of the Cell and Tissue Research Group, Walailak University, Nakhon Si Thammarat 80161, Thailand.
authors.forename: Phanit
authors.initials: P
authors.lastname: Koomhin
authors.affiliation: School of Medicine, Walailak University, Nakhon Si Thammarat 80161, Thailand; The Pathobiology of the Cell and Tissue Research Group, Walailak University, Nakhon Si Thammarat 80161, Thailand.
authors.forename: Chuchard
authors.initials: C
authors.lastname: Punsawad
authors.affiliation: School of Medicine, Walailak University, Nakhon Si Thammarat 80161, Thailand; The Pathobiology of the Cell and Tissue Research Group, Walailak University, Nakhon Si Thammarat 80161, Thailand.
authors.forename: Prasit
authors.initials: P
authors.lastname: Na-Ek
authors.affiliation: School of Allied Health Sciences and Public Health, Walailak University, Nakhon Si Thammarat 80161, Thailand; The Pathobiology of the Cell and Tissue Research Group, Walailak University, Nakhon Si Thammarat 80161, Thailand.
authors.forename: Apsorn
authors.initials: A
authors.lastname: Sattayakhom
authors.affiliation: Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
authors.forename: Prasit
authors.initials: P
authors.lastname: Suwannalert
keywords: alcoholic steatosis; heme oxygenase-1; hemin; oxidative stress; zinc protoporphyrin IX