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AbstractThe recovery of skin wounds is a complex biological process involving three basic mechanisms: inflammatory phase, re-epithelialization followed by granulation and tissue remodeling. The interactions between inflammatory cells, fibroblasts, and keratinocytes induce microenvironmental changes at the wound site. Tissue remodeling is initiated by matrix-producing proteins and protease enzymes and collagen fibers in the dermis. A saponin extracted from ginseng, known as ginsenoside, has been shown to accelerate neovascularization in burn wounds in mice. It also increases levels of vascular endothelial growth factor and interleukin (IL-β). IL-β accelerate wound healing by promoting accumulation of macrophages at skin wound sites. Saponins are major active constituents of ginseng. They contain many ginsenosides. The purified ginsenosides or the extracts of ginseng root have been reported to have beneficial effects on damaged skin. For instance, red ginseng root extract protected skin from acute UVB-irradiation. Ginsenoside F1, an enzymatically modified derivative of the ginsenoside Rg1, protected HaCaT against UVB-induced apoptosis. Panax ginseng root extract promotes type I collagen synthesis in human dermal fibroblasts (HDF) via the Smad activation pathway and exhibits antioxidant activity against free radicles including diphenyl-p-picrylhydrazyl treatment. In addition, ginsenoside Rb1 promotes healing process of burn wound by enhancing angiogenesis. Among the various ginsenosides, ginsenoside Rb1 has been found to most potent agent for wound healing.
CitationSethi Chopra, D., Gupta, A., Singh, D. and Singh, N. (2022) Anti-inflammatory potential of ginseng for wound healing, in Hano, C. and Chen, J-T (Eds.) Ginseng - modern aspects of the famed traditional medicine. London: IntechOpen.
TypeChapter in book
Description© 2022 The Authors. Published by IntechOpen. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://www.intechopen.com/chapters/79331
Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/3.0/