Daidzein stimulates collagen synthesis by activating the TGF ‐β/smad signal pathway

Hozzein

Journal Cellular Physiology

et al. 2016

Multiple mechanisms contribute to impaired diabetic wound healing including impaired neovascularization and deficient endothelial progenitor cell (EPC) recruitment. Bee venom (BV) has been used as an anti-inflammatory agent for the treatment of several diseases. Nevertheless, the effect of BV on the healing of diabetic wounds has not been studied. Therefore, in this study, we investigated the impact of BV on diabetic wound closure in a type I diabetic mouse model. Three experimental groups were used: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated with BV. We found that the diabetic mice exhibited delayed wound closure characterized by a significant decrease in collagen production and prolonged elevation of inflammatory cytokines levels in wounded tissue compared to control non-diabetic mice. Additionally, wounded tissue in diabetic mice revealed aberrantly up-regulated expression of ATF-3 and iNOS followed by a marked elevation in free radical levels. Impaired diabetic wound healing was also characterized by a significant elevation in caspase-3, -8, and -9 activity and a marked reduction in the expression of TGF-β and VEGF, which led to decreased neovascularization and angiogenesis of the injured tissue by impairing EPC mobilization. Interestingly, BV treatment significantly enhanced wound closure in diabetic mice by increasing collagen production and restoring the levels of inflammatory cytokines, free radical, TGF-β, and VEGF. Most importantly, BV-treated diabetic mice exhibited mobilized long-lived EPCs by inhibiting caspase activity in the wounded tissue. Our findings reveal the molecular mechanisms underlying improved diabetic wound healing and closure following BV treatment. J. Cell. Physiol. 231: 2159-2171, 2016. © 2016 Wiley Periodicals, Inc.

Section: Discussionmentioning

confidence: 99%

Bee Venom Accelerates Wound Healing in Diabetic Mice by Suppressing Activating Transcription Factor‐3 (ATF‐3) and Inducible Nitric Oxide Synthase (iNOS)‐Mediated Oxidative Stress and Recruiting Bone Marrow‐Derived Endothelial Progenitor Cells

Hozzein

Journal Cellular Physiology

et al. 2016

Section: Regulatory Effect Of Usm On Tgf-β1/smad Pathwaymentioning

confidence: 99%

“…TGF-β is the major activator of collagen synthesis in human skin fibroblasts. The TGF-β type 1 receptor initiates the synthesis of type 1 procollagen [39]. UV irradiation impairs TGF-β and Smad2/3 signaling, decreasing type 1 procollagen synthesis, and leads to the loss of collagen in the dermis [11].…”

Section: Regulatory Effect Of Usm On Tgf-β1/smad Pathwaymentioning

confidence: 99%

Protective Effects of Unsaponifiable Matter from Perilla Seed Meal on UVB-induced Damages and the Underlying Mechanisms in Human Skin Fibroblasts

et al. 2019

Unsaponifiable matter (USM) from perilla seed meal contains numerous phytochemicals, including tocopherols, phytosterols, squalene, and policosanols, that exhibit antioxidant and health-promoting properties. In this study, the protective effects of USM on UVB-induced skin aging were investigated in Hs68 cells. UVB irradiation decreased cell viability by 26% compared to the control. However, USM blocked UVB-induced cytotoxicity. Moreover, USM treatment significantly decreased the UVB-induced production of reactive oxygen species and attenuated the UVB-induced production and mRNA expression of matrix metalloproteinases (MMPs) by inhibiting the phosphorylation of mitogen-activated protein kinases and activator protein 1 (AP-1). Furthermore, UVB exposure led to a 49.4% reduction in collagen synthesis. However, USM treatment restored collagen synthesis through upregulation of the transforming growth factor beta (TGF-β)/Smad2/3 pathways. These data indicate that USM regulates the production of MMPs and collagen by modulation of the TGF-β/Smad pathway and AP-1 activity, suggesting that USM may be a useful anti-photoaging ingredient.

Afr. J. Trad. Compl. Alt. Med.

“…It has been demonstrated in vitro and in vivo that daidzein promoted collagen deposition by stimulating collagen synthesis via up-regulating the expression of type I pro-collagen and inhibiting collagen degradation via down-regulating the levels of MMP1 (matrix metalloproteinase1), and MMP2. This collagen metabolic regulation was mediated by TGF-β/smad signal pathway, phosphorylated-smad2, smad3 and TGF-β was significantly higher in the daidzein-treated cells when compared to the control (Zhao et al, 2015). Exposure to solar UV radiation for a long time, in particular UVB radiation, accelerates skin aging due to induced production of oxygen free radicals in a study of pig skin model which is similar to the human skin.…”

Section: Anti-aging Activitymentioning

confidence: 83%

Daidzein: A review of pharmacological effects

Sun¹,

Ye²,

Liu³

et al. 2016