Pre-clinical evidences of Pyrostegia venusta in the treatment of vitiligo.

[1]  C. Antoniou,et al.  Stimulated human melanocytes express and release interleukin‐8, which is inhibited by luteolin: relevance to early vitiligo , 2014, Clinical and experimental dermatology.

[2]  P. Płonka,et al.  HGF/SF Increases Number of Skin Melanocytes but Does Not Alter Quality or Quantity of Follicular Melanogenesis , 2013, PloS one.

[3]  A. Xu,et al.  A mouse model of vitiligo induced by monobenzone , 2013, Experimental dermatology.

[4]  M. Mansuri,et al.  Vitiligo: interplay between oxidative stress and immune system , 2013, Experimental dermatology.

[5]  M. Otuki,et al.  Hyperpigmentant activity of leaves and flowers extracts of Pyrostegia venusta on murine B16F10 melanoma. , 2012, Journal of ethnopharmacology.

[6]  S. Orlow,et al.  Vitiligo inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8 , 2012, The Journal of investigative dermatology.

[7]  Poonam Sharma,et al.  In vivo antioxidative property, antimicrobial and wound healing activity of flower extracts of Pyrostegia venusta (Ker Gawl) Miers. , 2012, Journal of ethnopharmacology.

[8]  Lidiane S. Franqui,et al.  Anti-inflammatory and antinociceptive effects of the hydroethanolic extract of the flowers of Pyrostegia venusta in mice , 2012 .

[9]  F. Souza-Fonseca-Guimaraes,et al.  Effectiveness of Vernonia scorpioides ethanolic extract against skin inflammatory processes. , 2011, Journal of ethnopharmacology.

[10]  C. Melief,et al.  Monobenzone‐induced depigmentation: from enzymatic blockade to autoimmunity , 2011, Pigment cell & melanoma research.

[11]  B. Longley,et al.  Topical application of bleaching phenols; in-vivo studies and mechanism of action relevant to melanoma treatment , 2011, Melanoma research.

[12]  S. Glassman.  Vitiligo, reactive oxygen species and T-cells. , 2011, Clinical science.

[13]  Lidiane S. Franqui,et al.  Pyrostegia venusta attenuate the sickness behavior induced by lipopolysaccharide in mice. , 2010, Journal of ethnopharmacology.

[14]  M. Sprangers,et al.  The burden of vitiligo: patient characteristics associated with quality of life. , 2009, Journal of the American Academy of Dermatology.

[15]  M. Picardo,et al.  Clinical practice. Vitiligo. , 2009, The New England journal of medicine.

[16]  Rebat M Halder,et al.  Vitiligo update. , 2009, Seminars in cutaneous medicine and surgery.

[17]  Wen‐yuan Zhu,et al.  The use of botanical extracts as topical skin-lightening agents for the improvement of skin pigmentation disorders. , 2008, The journal of investigative dermatology. Symposium proceedings.

[18]  I. Kawase,et al.  Glycine inhibits melanogenesis in vitro and causes hypopigmentation in vivo. , 2007, Biological & pharmaceutical bulletin.

[19]  Shyamali Roy.  Melanin, Melanogenesis, and Vitiligo , 2007 .

[20]  U. Kisa,et al.  Increased tumor necrosis factor alpha (TNF‐α) and interleukin 1 alpha (IL1‐α) levels in the lesional skin of patients with nonsegmental vitiligo , 2006 .

[21]  U. Kisa,et al.  Increased tumor necrosis factor alpha (TNF-alpha) and interleukin 1 alpha (IL1-alpha) levels in the lesional skin of patients with nonsegmental vitiligo. , 2006, International journal of dermatology.

[22]  M. Ichihashi,et al.  Down-regulation of Melanogenesis by Phospholipase D2 through Ubiquitin Proteasome-mediated Degradation of Tyrosinase* , 2004, Journal of Biological Chemistry.

[23]  B. Gilchrest,et al.  Topical application of a protein kinase C inhibitor reduces skin and hair pigmentation. , 2004, The Journal of investigative dermatology.

[24]  J. Arnhold,et al.  Properties, Functions, and Secretion of Human Myeloperoxidase , 2004, Biochemistry (Moscow).

[25]  T. Hayashi,et al.  Central role of defective apoptosis in autoimmunity. , 2003, Journal of molecular endocrinology.

[26]  M. Mockenhaupt,et al.  Tumor necrosis factor alpha induces upregulation of CXC-chemokine receptor type II expression and magnifies the proliferative activity of CXC-chemokines in human melanocytes. , 2003, European journal of dermatology : EJD.

[27]  S. Moretti,et al.  New insights into the pathogenesis of vitiligo: imbalance of epidermal cytokines at sites of lesions. , 2002, Pigment cell research.

[28]  J. She,et al.  Genetic association of the catalase gene (CAT) with vitiligo susceptibility. , 2002, Pigment cell research.

[29]  H. Tagami,et al.  Mediators of inflammation involved in UVB erythema. , 2000, Journal of dermatological science.

[30]  R. Braz-Filho,et al.  Chemical constituents from roots of Pyrostegia venusta and considerations about its medicinal importance , 2000 .

[31]  D. Flaherty,et al.  Dihydrofluorescein diacetate is superior for detecting intracellular oxidants: comparison with 2',7'-dichlorodihydrofluorescein diacetate, 5(and 6)-carboxy-2',7'-dichlorodihydrofluorescein diacetate, and dihydrorhodamine 123. , 1999, Free radical biology & medicine.

[32]  K. Schallreuter.  Successful Treatment of Oxidative Stress in Vitiligo , 1999, Skin Pharmacology and Physiology.

[33]  O. Damour,et al.  Modulation of normal human melanocyte dendricity by growth-promoting agents. , 1993, Pigment cell research.

[34]  J. Exton,et al.  Activation of phospholipase D by protein kinase C. Evidence for a phosphorylation-independent mechanism. , 1992, Journal of Biological Chemistry.

[35]  P. Stanley,et al.  Mouse skin inflammation induced by multiple topical applications of 12-O-tetradecanoylphorbol-13-acetate. , 1991, Skin pharmacology : the official journal of the Skin Pharmacology Society.

[36]  D. Priebat,et al.  Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. , 1982, The Journal of investigative dermatology.