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Beta-glucans, which existed in the cell walls of cereals, bacteria, and fungi, comprise a group of β- d -glucose polysaccharides. We investigated the effects of four kinds of beta-glucan, that are derived from barley, yeast, mushroom, and euglena on wound healing. The migration and viability of keratinocyte or fibroblast were analyzed using the in vitro scratch wound healing assay, invasion assay, MTT assay, and in vivo assay. All the beta-glucans had a significant effect on keratinocyte migration at 20 μM and showed no toxicity on dermal fibroblast. Moreover, treatment of keratinocytes with the beta-glucan derived from the mushroom ( Schizophyllum commune ) promoted in vivo wound closure. The Integrin/FAK/Src pathway is known to affect cell migration by forming lamellipodia. Beta-glucan from S. commune activates the Integrin/FAK/Src signaling pathway in a time-dependent. Reactive oxygen species are associated with fibroblast differentiation to contract dermal layer and synthesize collagens. We found that fibroblast was activated by increasing NOX4 expression. We propose that beta-glucan derived from mushroom is capable of promoting keratinocyte migration via the induction of FAK/Src phosphorylation there by accelerating wound closure and activating dermal fibroblast differentiation through NADPH oxidase for matrix remodeling.

Keratinocyte-fibroblast interactions are critical for skin repair after injury. During the proliferative phase of wound healing, proliferation, migration and differentiation of these cells are the major mechanisms leading to tissue remodeling. We have previously reported that glycitin, a major soy isoflavone, stimulates dermal fibroblast proliferation; and the phytochemical, 4′,6,7-trimethoxyisoflavone (TMF), induces migration of HaCaT keratinocyte cells. We therefore investigated whether these compounds display synergistic effects on skin cells during wound healing in vitro and in vivo. Co-treatment with TMF and glycitin synergistically promotes the proliferation and migration of both keratinocytes and dermal fibroblasts, with a 1:1 ratio of these compounds showing the greatest efficacy in our co-culture system. This keratinocyte-fibroblast interaction occurred via the secretion of TGF-β, and the induction of differentiation and proliferation was confirmed in both indirect and direct co-culture assays. In an excisional and burn wound animal model, mice treated with a 1:1 ratio of TMF and glycitin showed faster wound closure, regeneration and scar reduction than even the positive control drug. These data indicate that two isoflavones, TMF and glycitin, act synergistically to promote wound healing and anti-scarring and could potentially be developed together as a bioactive therapeutic for wound treatment. KCI Citation Count: 39

Exposure of strong and repeated UV on the skin leads to skin aging, characterized with wrinkling, sagging, dyspigmentation, and laxity. Numerous studies revealed that Matrix metalloproteinases are related to skin aging and functions as degrading enzyme of various types of collagen. Here, we attempted to evaluate the effectiveness of glycitin (4′-hydroxy-6-methoxyisoflavone- 7-d-glucoside) on skin aging and mechanisms of action in UV-irradiated human dermal fibroblasts. Especially we focused on the expression of Matrix metalloproteinase-1 (MMP-1), which degrades procollagen type-I in dermis, by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, and reverse transcription polymerase chain reaction in cell lysates or media. Our results showed that glycitin increased the viability of human dermal fibroblast and alleviated MMP-1 expression caused by UV irradiation. In addition, synthesis of type-I collagen was increased and UV-induced phosphorylation of ERK/JNK/p38 was decreased in dose-dependent manners. Taken together, we demonstrated that treatment with glycitein have a protective effect on skin aging by inhibiting of MMP-1 and increasing of collagen through ERK/JNK/P38 down-regulation, which may be mediated by the inhibition of ERK, JNK, and p38 mitogen-activated protein kinases. We suggest that glycitin is a potential agent for the treatment of skin ageing.