Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/30269
Title: Effects of Hydrogen Peroxide on Different Models of Wound Healing
Authors: LOO ENG KIAT ALVIN
Keywords: Wound healing, hydrogen peroxide, H2O2, ROS, oxidative damage, MAPK
Issue Date: 17-Aug-2011
Source: LOO ENG KIAT ALVIN (2011-08-17). Effects of Hydrogen Peroxide on Different Models of Wound Healing. ScholarBank@NUS Repository.
Abstract: It has been established that low concentrations of H<sub>2</sub>O<sub>2</sub> are produced in wounds. Yet at the same time, there is evidence that excessive oxidative damage is correlated with chronic wounds. In this thesis we explored the effects of H<sub>2</sub>O<sub>2</sub> in keratinocyte cell culture models and an <i>in vivo</i> excision wound model of wound healing. H<sub>2</sub>O<sub>2</sub> stimulates a persistent ERK phosphorylation in HaCaT keratinocytes which was found to be important in cell proliferation and migration. H<sub>2</sub>O<sub>2</sub> also increases the production of proinflammatory and pro-angiogenic cytokines such as Vascular endothelial growth factor, Interleukin-8, Granulocyte-macrophage colony-stimulating factor, Tumor necrosis factor-a, interleukin-6 and Interferon gamma-induced protein 10, in HaCaT keratinocytes. H<sub>2</sub>O<sub>2</sub> was found to increase re-epithelialization in a primary fibroblast-keratinocyte co-culture model as well. In a C57BL/6 mice excision wound model, low concentrations of H<sub>2</sub>O<sub>2</sub> (10 mM) were found to enhance angiogenesis while high concentrations of H<sub>2</sub>O<sub>2</sub> (166 mM) retarded wound closure and connective tissue formation. High concentrations of H<sub>2</sub>O<sub>2</sub> also increased the levels of MMP-8 in the wounds, which could be the cause of reduced connective tissue formation. Wounding was found to increase oxidative lipid damage, as measured by F<sub>2</sub>-isoprostanes, but H<sub>2</sub>O<sub>2</sub> treatment does not significantly increase it even at concentrations that delay wound healing. This challenges the putative claim that oxidative damage contributes to the pathology of poor healing wounds.
URI: http://scholarbank.nus.edu.sg/handle/10635/30269
Appears in Collections:Ph.D Theses (Open)

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