Shikonin promotes intestinal wound healing in vitro via induction of TGF-β release in IEC-18 cells

Abstract

The intestinal barrier is a complex system with a dynamic structure that is designed for the maintenance of homeostasis in healthy individuals. Ulcerative colitis, one of the main manifestations of inflammatory bowel disease, is characterized by an inadequate and delayed wound healing. Shikonin, the active principle in the root of Lithospermum erythrorhizon, has demonstrated its ability to attenuate dextran sulfate sodium-induced ulcerative colitis in mice. Moreover, the root of L. erythrorhizon has been used in traditional Chinese medicine for treatment of burns, anal ulcers, hemorrhoids and skin wounds. However, the effect of shikonin on intestinal wound healing is unknown. Using an in vitro model for wound healing, we observed that shikonin enhances cell migration of intestinal epithelial cells through a mechanism that involves TGF-β1 induction. The combination of shikonin's anti-inflammatory activity together with its wound-healing properties makes it a great potential therapeutic agent for the treatment of injury associated with intestinal inflammation.

Keywords: 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenil-tetrazolium bromide; BSA; CD; Crohn’s disease; DMEM; DSS; Dulbecco’s Modified Eagle’s Medium; IBD; IEC-18 cells; MTT; NF-κB; PBS; STAT3; Shikonin; TGF; TGF-β; UC; Ulcerative colitis; Wound healing; bovine serum albumin; dextran sulfate sodium; inflammatory bowel disease; nuclear factor-κB; phosphate buffered saline; signal transducer and activator of transcription 3; transforming growth factor; ulcerative colitis.