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  • 2005-2009  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc.
    Wound repair and regeneration 13 (2005), S. 0 
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Tissue repair and wound healing are complex processes that involve inflammation, granulation, and tissue remodeling. Angiogenesis plays a central role in wound healing. Previously, we have shown that picroliv, a natural product obtained from the roots of Picrorhiza kurrooa upregulates the expression of vascular endothelial growth factor (VEGF) in human umbilical vein endothelial cells and insulin like growth factor (IGF) in rats during hypoxia (Cellular and Molecular Life Sciences 1999; 56: 348–55). In the present study, we have investigated the effect of Picroliv in an ex vivo rat aorta ring model of angiogenesis. Picroliv enhanced the sprouting and migration of endothelial cells. In this study, we have investigated the effect of picroliv in both unimpaired and dexamethasone (DX)-induced impaired cutaneous healing in a full thickness punch wound model in rats. The animals in the impaired healing group having been pretreated with DX. We studied the tissues by histology and morphometry. The data showed picroliv treatment resulted in improved reepithelialization, neovascularization, and migration of various cells such as endothelial, dermal myofibroblasts, and fibroblasts into the wound bed. Immunohistochemical localization showed an increased VEGF and alpha smooth muscle actin staining consistent with increased number of micro vessels in granulation tissue. These findings suggest that picroliv accelerated wound repair and thus could be developed as a therapeutic angiogenic agent for the wound healing.(This work was supported by a grant (5 R21 AT000517-02) from the NCCAM, National Institute of Health, Bethesda, MD.)
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc.
    Wound repair and regeneration 13 (2005), S. 0 
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Wound healing is a complicated biological process that involves interactions of multiple cell types, various growth factors, their mediators and the extracellular matrix proteins. In this study, we have studied the differential regulation of angiogenic genes during wound healing in transgenic diabetic mice and non-diabetic mice. One 8 mm full thickness cutaneous wound under aseptic conditions was created on either side of the midline. Wound tissues were studied at 4, 7, and 11 days postwounding and healing was assessed by histology. The pathway specific gene expression profile of wound tissue in transgenic diabetic mice was compared with the normal mice. Profiling of these genes showed differential regulation of many angiogenic promoters, inhibitors, growth factors and cytokines. Furthermore, in our study hypoxia inducible factor (HIF-1a), osteopontin (OPN) and osteonectin are induced early at day 4, in both the diabetic and nondiabetic wound. The expression was downregulated by 11-day postwounding in the nondiabetic wound, whereas diabetic wounds showed constitutively high expression of these genes. The expression patterns of these genes were concomitant with the extent of healing as assessed by histology at different time point postwounding. These results suggest wound healing is a complex process that involves cascade of interaction of various factors. Although a single gene may not be solely responsible for any impairment in healing; however, an in-depth study of these genes and precise balance between the inducers and inhibitors of angiogenesis may provide an answer to the delayed healing in diabetic conditions.(This work was supported by a grant (5 R21 AT000517-02) from the NCCAM, National Institute of Health, Bethesda, MD.)
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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