LONDON A compound found in the common curry spice turmeric appears to delay the liver damage that eventually causes cirrhosis, scientists said on Wednesday.
In a study published in Gut, a British Medical Journal title, Austrian scientists found that feeding the compound curcumin to mice reduced the types of inflammation that can cause liver cell damage, blockage and scarring.
Previous research has suggested that curcumin, which gives turmeric its bright yellow colour, has anti-inflammatory and antioxidant properties which may be helpful in fighting disease.
Some studies have indicated it can suppress cancer tumours and that people who eat lots of curry may be less prone to the disease, although curcumin loses its anti-cancer attributes quickly when it is ingested.
The Austrian research team wanted to find out if curcumin could delay the damage caused by progressive inflammatory liver disease, including two conditions called primary sclerosing cholangitis and primary biliary cirrhosis.
Both of these conditions, which can be sparked by genetic faults or autoimmune disease, cause the liver's plumbing system of bile ducts to become inflamed, scarred, and blocked.
This can lead to major tissue damage and irreversible and ultimately fatal liver cirrhosis, they explained.
The team led by Michael Trauner of the Gastroenterology and Hepatology division at the Medical University Graz in Austria analysed tissue and blood samples from mice with chronic liver inflammation before and after adding curcumin to their diet for four or eight weeks.
They found the curcumin diet significantly reduced bile duct blockage and curbed liver cell damage and scarring by interfering with chemical signalling pathways involved in inflammation.
Although the research was at a very early stage, the scientists said it seemed to show that curcumin targets "several different parts of the inflammatory process" and could offer a "promising treatment in the future".
U.S. researchers said in 2007 they had found curcumin may help stimulate immune system cells in Alzheimer's disease.
(Reporting by Kate Kelland, editing by Noah Barkin)