22th IFSCC (International Federal of societies of cosmetic chemists) Conference; Rio de Janeiro, October 30 - November, 01, 2013.
Silva MS, Eberlin S, Oliveira SC, Ferreira FG, Queiroz MLS
Wound healing is a dynamic process involving a complex and orchestrated interaction of soluble mediators, extracellular matrix (ECM), blood and parenchymal cells. During the second week of healing, fibroblasts assume a myofibroblast phenotype bearing ?-smooth muscle actin (?-SMA). Myofibroblasts align themselves along the borders of the ECM to generate a constrictive force, facilitating wound closure. This event requires stimulation by growth factors, as transforming growth factor beta 1 (TGF-?1), which belongs to a family of growth factors involved in a number of processes in wound healing: inflammation, stimulating angiogenesis, fibroblast proliferation, collagen synthesis and deposition, and remodeling of the new extracellular matrix. Deregulation of TGF- ?1 signalling has been implicated in the development of fibroproliferative disorders resulting in alterations on target genes transcription involved in skin wound healing. Keloid and hypertrophic scars are defined as the end product of a chronic inflammatory process induced by a variety of stimuli that culminate in tissue overgrowth and hardening as a result of excessive collagen deposition. Keloid fibroblasts have a distinct phenotype and are more susceptible to the effects of multiple growth factors, cytokines and inflammatory mediators. Moreover, they present pronounced proliferative capacity and resistance to apoptosis. Compared with normal fibroblasts, keloid fibroblasts express high levels of TGF-?1, type I and III collagens, type 1 (T?R1) and 2 (T?RII) TGF-? receptors. Thus, inhibition of TGF-?1 signaling would be a potential therapeutic approach to prevent keloid and hypertrophic scar formation. Rhodiola rosea has been categorized as an adaptogen due to its proved ability to increase resistance to a variety of stressors. Studies performed in our laboratory demonstrated the ability of a R. rosea extract, standardized in rosavins (1.5%) and salidrosides (0.5%), to reestablish the altered levels of proinflammatory cytokines, proteinases and collagen in human keratinocyte and fibroblast cultures. In this study, we evaluated the in vitro effects of Rhodiola rosea extract (RRE) in the release of transforming growth factor-?1 by human skin fibroblasts and human skin explants. Human fibroblasts and human skin explants were incubated for 72 h with several RRE concentrations (3, 1.5 and 0.75mg/mL). The levels of growth factor were measured using commercial kits. Our results demonstrated that incubation with RRE at 1.5mg/mL produces a significant reduction (P<0,01, ANOVA, Tukey) in the release of TGF-?1 by human skin explants (19.65±15.87pg/mL) in relation to control group (413.2±19.65pg/mL). In the same way, RRE produced a reduction (179.8±1.058pg/mL) in the levels of TGF-?1 when compared to control group (480.0±20.69pg/mL). These data suggest that RRE can optimize the healing process by modulating the excessive deposition of collagen-induced TGF-?1, which would reduce the formation of fibroproliferative disorders such as keloid and hypertrophic scars. Studies to evaluate the production of ECM components, particularly collagen, metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) are in progress in our laboratory to confirm this hypothesis and define the exact mechanisms underlying to RRE effects.
Wound healing is a dynamic process involving a complex and orchestrated interaction of soluble mediators, extracellular matrix (ECM), blood and parenchymal cells. During the second week of healing, fibroblasts assume a myofibroblast phenotype bearing ?-smooth muscle actin (?-SMA). Myofibroblasts align themselves along the borders of the ECM to generate a constrictive force, facilitating wound closure. This event requires stimulation by growth factors, as transforming growth factor beta 1 (TGF-?1), which belongs to a family of growth factors involved in a number of processes in wound healing: inflammation, stimulating angiogenesis, fibroblast proliferation, collagen synthesis and deposition, and remodeling of the new extracellular matrix. Deregulation of TGF- ?1 signalling has been implicated in the development of fibroproliferative disorders resulting in alterations on target genes transcription involved in skin wound healing. Keloid and hypertrophic scars are defined as the end product of a chronic inflammatory process induced by a variety of stimuli that culminate in tissue overgrowth and hardening as a result of excessive collagen deposition. Keloid fibroblasts have a distinct phenotype and are more susceptible to the effects of multiple growth factors, cytokines and inflammatory mediators. Moreover, they present pronounced proliferative capacity and resistance to apoptosis. Compared with normal fibroblasts, keloid fibroblasts express high levels of TGF-?1, type I and III collagens, type 1 (T?R1) and 2 (T?RII) TGF-? receptors. Thus, inhibition of TGF-?1 signaling would be a potential therapeutic approach to prevent keloid and hypertrophic scar formation. Rhodiola rosea has been categorized as an adaptogen due to its proved ability to increase resistance to a variety of stressors. Studies performed in our laboratory demonstrated the ability of a R. rosea extract, standardized in rosavins (1.5%) and salidrosides (0.5%), to reestablish the altered levels of proinflammatory cytokines, proteinases and collagen in human keratinocyte and fibroblast cultures. In this study, we evaluated the in vitro effects of Rhodiola rosea extract (RRE) in the release of transforming growth factor-?1 by human skin fibroblasts and human skin explants. Human fibroblasts and human skin explants were incubated for 72 h with several RRE concentrations (3, 1.5 and 0.75mg/mL). The levels of growth factor were measured using commercial kits. Our results demonstrated that incubation with RRE at 1.5mg/mL produces a significant reduction (P<0,01, ANOVA, Tukey) in the release of TGF-?1 by human skin explants (19.65±15.87pg/mL) in relation to control group (413.2±19.65pg/mL). In the same way, RRE produced a reduction (179.8±1.058pg/mL) in the levels of TGF-?1 when compared to control group (480.0±20.69pg/mL). These data suggest that RRE can optimize the healing process by modulating the excessive deposition of collagen-induced TGF-?1, which would reduce the formation of fibroproliferative disorders such as keloid and hypertrophic scars. Studies to evaluate the production of ECM components, particularly collagen, metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) are in progress in our laboratory to confirm this hypothesis and define the exact mechanisms underlying to RRE effects.
