Researchers from Denmark and the US have shown that curcumin increases levels of a protein called cathelicidin anti-microcial peptide (CAMP) that has been shown to fight bacteria and direct body’s response to inflammation. Earlier research had demonstrated that vitamin D increases CAMP levels through its interaction with vitamin D receptors (VDRs) on the surfaces of cells. The new findings suggest that curcumin acts on CAMP through a different mechanism. The findings have appeared in the Journal of Nutritional Biochemistry. “Curcumin is consumed through turmeric in the diet at fairly low levels,” said Adrian Gombart, an associate professor of biochemistry at the Oregon State University in the US. “It is possible that sustained consumption over time may be healthy and may help protect against infection, especially in the stomach and the intestines,” Gombart said in a statement issued through the university. Studies on the biochemical effects of curcumin over the past two decades, mainly through animal experiments, have indicated that it has anti-inflammatory, anti-cancer, anti-oxidant and anti-infective properties. The study by Gombart and his colleagues, supported by a US National Institutes of Health grant, was part of an effort to determine the genetic or molecular mechanisms that might explain some of the effects attributed to curcumin. The Oregon scientists, collaborating with Neils Borregaard, professor of hematology at the University of Copenhagen in Denmark, designed a set of experiments to study how curcumin and polyunsaturated fatty acids might influence CAMP in human cells. They observed that polyunsaturated fatty acids had no impact on the levels of CAMP, while curcumin appeared to activate the CAMP gene and led to a statistically significant increase in CAMP levels. The effect of curcumin on CAMP levels appeared to be weaker than the effect of vitamin D on this protein, but its independent mechanism, Gombart said in a media release from the university, points to a new avenue for regulating CAMP.
Source : Telegraphindia
