A treatment for a major health problem may already be on the shelves of our pharmacies.
Liver fibrosis is a condition that affects hundreds of millions of individuals and progresses silently towards serious states like cirrhosis. Although research has been interested in it for a long time, no specific treatment has so far been approved to directly counteract it. A glimmer of hope is emerging from a surprising combination of two already widely used substances.
When the liver faces repeated damage, it initiates an abnormal repair process. Specialized cells, hepatic stellate cells, then come into play and produce collagen, leading to the appearance of scar tissue and, ultimately, irreversible degradation of the organ.
A team from the China Pharmaceutical University recently published its results in the journal
Targetome. This work demonstrates that combining silybin, a compound derived from milk thistle, and carvedilol, a medication for heart failure, produces a much more pronounced effect than each substance administered alone. This duo successfully hindered the activity of the cells responsible for the formation of scars.
To achieve this result, the researchers first evaluated the properties of silybin alone. It effectively protects liver cells, reduces oxidative stress, and soothes inflammation. However, its direct action on genes associated with fibrosis and the production of scar tissue proved to be limited. It therefore seems to operate mainly by protecting the organ, without interrupting the process that generates scars.
To amplify this effect, the scientists tested silybin in combination with approximately four hundred already approved drugs. Carvedilol stood out as the most effective partner. Administered together according to a specific dose ratio, these two molecules significantly reduced inflammation, liver damage, and collagen accumulation in animal models, performing better than a commonly used reference treatment in this field.
This synergy is explained by a joint action on a major cellular communication system. The combined treatment disrupts a signaling pathway that orders cells to produce fibrous tissue, thus preventing it from being triggered. This discovery charts a tangible therapeutic path, especially since both products already benefit from wide use, with established safety profiles and moderate cost.
This strategy, which relies on drug repurposing, could therefore offer an accelerated path towards future clinical trials.