These Korean researchers from Hallym University have identified a new mechanism, involving ginsenoside Rb1, an active ingredient in ginseng, capable of stimulating the migration of keratinocytes and promoting the healing of skin wounds. The study, presented in the Journal of Medicinal Food, thus reveals a new therapeutic approach and identifies new targets to boost epithelialization during the wound healing process.
The ginsenosides and saponins in ginseng are already documented for their antioxidant and immune-stimulating abilities. It has already been demonstrated that the ginsenosides present in a particular species of ginseng, Panax ginseng, modulate certain processes of tissue and cellular metabolism and immunity in such a way as to cause positive effects in several diseases, including diabetes, atherosclerosis, hyperlipidemia, hypertension and certain multiple cancers. To date, more than 30 molecular species of ginsenosides have been identified and some are already known to modify skin functions, such as the stimulation of collagen production with anti-aging and healing effects. However, the mechanisms underlying these beneficial biological effects of ginsenosides remain poorly understood.
Previous studies have shown that ginsenosides regulate the metabolism of sphingolipids, complex lipids that play a key role in signal transmission and recognition between cells. Other recent studies have demonstrated that sphingolipids also regulate wound healing processes as well as restoring epidermal barrier function during the wound healing process. Some will increase the expression of metalloproteases (MMPs), involved in the healing process. The scientists thus show that the alteration of sphingolipids induced by ginsenoside Rb1 itself induces an increased migration of keranocytes towards the site of the wound.
New possible therapeutic targets: The study, conducted in vitro on lines of human keratocytes, deciphers a hitherto unidentified Rb1 signaling mechanism which will facilitate the migration of keranocytes by the production of important migration factors, including a key target protein, S1P.
Finally, these results suggest that the modulation of S1P by pharmacological agents could promote and accelerate wound healing.
