WORCESTER, Mass., July 31 (UPI) -- Researchers found that two gout medications prevented mice in the lab from developing liver disease due to excessive consumption of alcohol.
The drugs focus on uric acid and adenosine triphosphate, or ATP, which are released by alcohol-damaged hepatocytes, causing inflammation and the development of liver disease.
"We are increasingly appreciating the central role of inflammation and immune responses in a variety of diverse diseases," said Dr. John Wherry, deputy editor of the Journal of Leukocyte Biology, in a press release. "The link between alcohol induced tissue damage and sensing by the immune system through the inflammasome opens the door for new therapeutics targeting this type of inflammation in liver diseases."
The researchers first isolated immune cells from human volunteers and exposed them to alcohol-treated human hepatocytes. They found indications of uric acid and ATP in test tubes after the exposure, as expected.
After confirming the presence of uric acid and ATP in the test tubes, researchers tested four groups of mice for signs of alcohol-related liver disease. The researchers gave one group of wild-type mice and one group deficient in the NLRP3 inflammasome component a chronic alcohol-containing diet, and gave groups of wild-type mice and NLRP3 deficient mice an alcohol-free diet.
The wild-type mice fed the chronic alcohol diet developed characteristics of alcoholic liver disease, including levels of "sterile danger molecules," uric acid and ATP. The NLRP3-deficient mice and the mice not on alcohol-free diets showed no signs of liver disease.
"This study should ultimately help patients with alcoholic liver disease to prevent or treat acute episodes of alcoholic hepatitis, a potentially lethal condition," said Dr. Gyongyi Szabo, in Department of Medicine at the University of Massachusetts Medical School.
The study is published in the Journal of Leukocyte Biology.