Washington: Antioxidants found in apple peels may lead to new treatments and therapies for people suffering from bowel inflammation disorders, according to a new research.
Oral ingestion of apple polyphenols can suppress T cell activation and improve experimental colitis in mice, the report said.
T cells are a type of blood cells, which play a key role in cell-mediated immunity and helps the body fight against diseases or harmful substances.
This study is the first to show a role for T cells in polyphenol-mediated protection against an autoimmune disease and could lead to new therapies and treatments for people with disorders related to bowel inflammation, such as ulcerative colitis, Crohn’s disease and colitis-associated colorectal cancer.
“Many people with colitis use some form of dietary supplement to complement conventional therapies, but most of the information on the health effects of complementary medicine remains anecdotal,” said David W. Pascual, Ph.D., a researcher involved in the work from the Department of Immunology and Infectious Diseases at Montana State University in Bozeman, Montana.
“Also, little is known about exactly how these therapies work, if they work at all.”
“Our results show that a natural product found in apple peels can suppress colonic inflammation by antagonizing inflammatory T cells to enhance resistance against autoimmune disease.”
To make this discovery, scientists used a chemically induced model of colitis with Dextran sulfate sodium (DSS), researchers administered an oral placebo to one group of mice, and the other group of mice was given an oral dose of apple polyphenols every day during the course of the disease.
Results showed that mice treated orally with apple polyphenols were protected from colitis. Importantly, scientists also found that the treated mice had fewer activated T cells in their colons.
In mice lacking T cells, apple polyphenols were unable to protect against colitis or suppress proinflammatory cytokine expression, indicating apple polyphenols protect against colitis via the suppression of T cell activation and/or recruitment.