Dendrobium officinale Orchid Extract could improve wound healing in diabetic mice

Background In diabetes, delayed wound healing is one of the most prominent clinical manifestations and lacks satisfactory therapeutic schemes. Persistent inflammation impairs the healing process which occurs in the late phase of wound healing in diabetes mellitus (DM) mice. It has been report that dendrobium officinale (DE) could decrease inflammation and the NF-κB signaling pathway plays a critical role in regulated inflammation. The aim of the present study is to detect whether DE attenuated inflammation by NF-κB to accelerate wound healing in diabetes. Methods Mice were induced to diabetes by streptozocin (STZ) for 15 days. Two circular 8-mm full-thickness wounds were created on the back and then received DE treatment for 18 days. The percentage of wound healing, re-epithelialization and collagen deposition were calculation to evaluation the effect of DE on wound healing. The expression levels of interleukin (IL)- 1β and TNF-α in the wound site were determined by WB. Macrophage deposition and the type of macrophage were detected by WB and immunohistochemical staining. In addition, the expression of p65 was detected by WB. Results Herein, we observed that the late wound healing could be improved by dendrobium officinale orchid extract (DE) in streptozotocin (STZ)-induced DM mice. The accumulation of collagen was increased by DE treatment in the skin. We also found that the expression of pro-inflammation cytokines IL-1β, and TNF-α were inhibited by DE treatment in the skin wounds of DM mice. Furthermore, the macrophages accumulation which increased in diabetes wound site, were inhibited by DE treatment in the DM mice wound skin. And the CD163 which is a marker of type 2 macrophage was increased by DE treatment. Moreover, we confirmed that DE could decrease the expression of iNos which is a marker of type 1 macrophage by IHC in the skin wounds. And the levels of p65 and p65 phosphorylation were decreased by DE. Conclusions Wound healing can be improved by DE through NF-κB signaling pathway to attenuated inflammation in STZ-induced diabetic mice.