A pair of new research papers have shown that silibinin – a compound found primarily in milk thistle extract – could help to protect against certain forms of skin cancer by boosting skin cells defenses against ultraviolet (UV) radiation.
"When you have a cell affected by UV radiation, you either want to repair it or kill it so that it cannot go on to cause cancer. We show that silibinin does both." explained Professor Rajesh Agarwal.
Killing affected cells
The first study, published in the journal Photochemistry and Photobiology (found here) worked with human skin cells subjected to UVA radiation, which makes up around 95% of the sun's radiation.
Agarwal and his team treated the UVA-affected cells with silibinin – discovering that when the milk thistle compound was applied the rate at which these damaged cells died increased dramatically. This essentially means that the compound is removing the mutated cells that can cause skin cancer and photo-aging, said the researcher.
"When you take human skin cells – keratinocytes – and treat them with silibinin, nothing happens. It's not toxic.” said Agarwal.
“But when you damage these cells with UVA radiation, treatment with silibinin kills the cells," he confirmed.
Specifically, the study shows that pretreatment with silibinin resulted in higher release of reactive oxygen species (ROS) within the UVA-exposed cells, leading to higher rates of cell death, the researchers explained.
In a second study from the same team –published in Molecular Carcinogenesis (found here) – silibinin is also found to protect healthy cells from becoming damaged by UV radiation in the first instance, they explain.
This study used UVB radiation, which accounts for the other 5% of the sun’s radiation, finding that rather than helping to kill cells that become damaged (as it did with UVA radiation) silibinin application leads to protection of skin cells by up-regulating the expression of interleukin-12(IL-12) which works to quickly repair damaged cells.
“In view of the fact that an enhanced endogenous IL-12 level could effectively remove UVB-caused DNA damage and associated skin cancer, our findings suggest that the use of silibinin in UVB-damaged human skin would also be a practical and translational strategy to manage solar radiation-caused skin damages as well as skin cancer,” said the authors.
Agarwal reiterated that prevention of UV-induced skin cancer can happen in two ways: by protecting against DNA damage or by killing cells with damaged DNA. In silibinin, he said that there is a compound that works on both fronts.
With UVA, silibinin kills; with UVB, it protects by increasing cell repair mechanisms, he confirmed.
"It has been 20 years of work with this compound, silibinin," said Agarwal. "We first noticed its effectiveness in treating both skin and solid cancers, and we now have a much more complete picture of the mechanisms that allow this compound to work."
Agarwal and his colleagues said that they will continue to test the effectiveness of silibinin in cancer prevention and treatment in cell lines and mouse models, and are currently working toward human trials involving silibinin.