Study on the pathogenesis of liver injury caused by alcohol and drugs

Sang-Hoon Kim; Il-Gyu Ko; Jun-Jang Jin; Lakkyong Hwang; Bo-Kyun Kim; Seung-Soo Baek

doi:10.12965/jer.2142530.265

Study on the pathogenesis of liver injury caused by alcohol and drugs

J Exerc Rehabil. 2021 Oct 26;17(5):319-323. doi: 10.12965/jer.2142530.265. eCollection 2021 Oct.

Authors

Sang-Hoon Kim^{1

2}, Il-Gyu Ko², Jun-Jang Jin², Lakkyong Hwang², Bo-Kyun Kim³, Seung-Soo Baek¹

Affiliations

¹ Department of Sport & Health Sciences, College of Art & Culture, Sangmyung University, Seoul, Korea.
² Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea.
³ Department of Emergency Technology, College of Health Science, Gachon University, Incheon, Korea.

Abstract

In the present study, alcohol, lipopolysaccharide (LPS), and carbon tetrachloride (CCL₄) were administered to experimental mice. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 concentrations, and collagen type 1alpha (COL-1A) and fibronectin expressions were measured to evaluate pathophysiology of liver injury. Levels of ALT and AST were significantly increased by alcohol treatment. Alcohol with LPS treatment increased ALT and AST levels more than alcohol alone treatment, but it was not statistically significant. Alcohol with CCL₄ treatment significantly increased ALT and AST levels more than alcohol alone treatment. Alcohol with LPS and CCL₄ treatment significantly increased ALT and AST levels more than alcohol with CCL₄ treatment. Concentrations of TNF-α, IL-1β, and IL-6 were significantly enhanced by alcohol treatment. Alcohol with LPS treatment significantly enhanced concentrations of TNF-α, IL-1β, and IL-6 more than alcohol alone treatment. Alcohol with CCL₄ treatment significantly enhanced TNF-α, IL-1β, and IL-6 concentrations more than alcohol alone treatment. Alcohol with LPS and CCL₄ treatment increased TNF-α, IL-1β, and IL-6 concentrations more than alcohol with CCL₄ treatment, but it was not statistically significant. COL-1A and fibronectin expressions were significantly increased by alcohol treatment. Alcohol with LPS treatment significantly increased COL-1A and fibronectin expressions more than alcohol alone treatment. Alcohol with CCL₄ treatment significantly increased COL-1A and fibronectin expressions more than alcohol alone treatment. Alcohol with LPS and CCL₄ treatment increased COL-1A and fibronectin expressions more than alcohol with CCL₄ treatment, but it was not statistically significant.

Keywords: Alcohol; CCL4; Lipopolysaccharide; Liver injury.