Psoriasis

Psoriasis is a chronic (long-lasting) skin disease characterized by scaling and inflammation. Scaling occurs when cells in the outer layer of the skin reproduce faster than normal and pile up on the skin’s surface.

Nutrients to fight psoriasis

Silymarin, Curcumin, OptiBerry, MSM, Omega 3's, Green tea extracts, vitamin D3, resveratrol.

In vivo assessment of iron and ascorbic acid in psoriatic dermis.

Leveque N, Robin S, Muret P, Mac-Mary S, Makki S, Berthelot A, Kantelip JP, Humbert P.
Laboratory of Cutaneous Bioengineering, Faculty of Medicine and Pharmacy, Besançon, France. Acta Derm Venereol. 2004;84(1):2-5
Reactive oxygen species play an important role in inflammatory skin diseases such as psoriasis. Reactive oxygen species synthesis is catalysed by iron and some species are scavenged by ascorbic acid. The aim of this work was to assess iron and ascorbic acid in uninvolved and involved psoriatic dermis and to compare the corresponding concentrations in the dermis of healthy subjects. Microdialysis associated with atomic absorption spectrometry and gas chromatography-mass spectrometry was used to assess iron and ascorbic acid, respectively. Seven psoriatic patients and five healthy volunteers were studied. Iron concentrations in the involved (57.1 +/- 19.3 microg/l) and uninvolved (49.7 +/- 27.1 microgl/l) psoriatic dermis were higher than the corresponding value determined in the dermis of healthy subjects (21.8 +/- 2.4 microg/l) (p<0.05). Ascorbic acid in involved (47.3 +/- 8.2 microg/ml) and uninvolved (42.0 +/- 14.0 microg/ml) psoriatic dermis was statistically lower than that found in healthy dermis (176.8 +/- 29.0 microg/ml) (p<0.05). These results demonstrate that psoriatic patients exhibit high iron and low ascorbic acid concentrations in the dermis, but there were no significant differences between involved and uninvolved skin.

Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to enhance antiangiogenic effects of EGCG through activation of FOXO transcription factor.

Shankar S, Chen Q, Srivastava RK. J Mol Signal. 2008 Mar 20;3:7.
Department of Biochemistry, University of Texas Health Science Center at Tyler, Tyler, Texas, 75708-3154, USA. rakesh.srivastava@uthct.edu.


ABSTRACT: BACKGROUND: We have recently shown that epigallocatechin-3-gallate (EGCG), a polyphenolic compound from green tea, inhibits angiogenesis. However, the molecular mechanisms by which EGCG inhibits angiogenesis have never been investigated. In this study, we examined the interaction of PI3K/AKT and MEK/ERK pathways on the regulation of FOXO transcription factors, which ultimately control the antiangiogenic effects of EGCG.

RESULTS: Inhibition of PI3K/AKT and MEK/ERK pathways interact synergistically to inhibit migration and capillary tube formation of HUVEC cells and further enhanced the antiangiogenic effects of EGCG. Inhibition of AKT and MEK kinases synergistically induced FOXO transcriptional activity, which was further enhanced in the presence of EGCG. Phosphorylation deficient mutants of FOXO induced FOXO transcriptional activity, inhibited HUVEC cell migration and capillary tube formation. Inhibition of FOXO phosphorylation also enhanced antiangiogenic effects of EGCG through transcriptional activation of FOXO.

CONCLUSION: Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to regulate antiangiogenic effects of EGCG through activation of FOXO transcription factors. The activation of FOXO transcription factors through inhibition of these two pathways may have physiological significance in management of diabetic retinopathy, rheumatoid arthritis, psoriasis, cardiovascular diseases, and cancer.


Green tea polyphenol induces caspase 14 in epidermal keratinocytes via MAPK pathways and reduces psoriasiform lesions in the flaky skin mouse model.

Hsu S, Dickinson D, Borke J, Walsh DS, Wood J, Qin H, Winger J, Pearl H, Schuster G, Bollag WB. Exp Dermatol. 2007 Aug;16(8):678-84.
Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, Medical College of Georgia, Augusta, GA 30912, USA. shsu@mail.mcg.edu


Psoriasis form lesions are characterized by hyperproliferation and aberrant differentiation of epidermal keratinocytes, accompanied by inflammation, leading to a disrupted skin barrier with an abnormal stratum corneum. The expression and proteolytic processing of caspase 14, a member of the caspase family which is associated with epithelial cell differentiation, planned cell death, and barrier formation, is altered in psoriatic epidermis. We recently reported that human psoriatic tissues lack normal expression of caspase 14 [J Dermatol Sci37 (2005) 61], and caspase 14 is induced by EGCG, a green tea polyphenol (GTP), in exponentially growing normal human epidermal keratinocytes (NHEK) [J Pharmacol Exp Ther315 (2005) 805]. This suggests that GTPs may have beneficial effects on psoriasiform lesions. The current study aimed to determine whether MAPK pathways are required for GTP-induced caspase 14 expression in NHEK and if GTPs can modulate the expression of pathological markers in the psoriasiform lesions that develop in the flaky skin mouse. The results indicate that the p38 and JNK MAPK pathways are required for EGCG-induced expression of caspase 14 in NHEK. Importantly, topical application of 0.5% GTPs significantly reduced the symptoms of epidermal pathology in the flaky skin mice, associated with efficient caspase 14 processing and reduction in proliferating cell nuclear antigen levels. This suggests that GTP-activated pathways may be potential targets for novel therapeutic approaches to the treatment of some psoriasiform skin disorders.

Vitamin D therapy in psoriasis.

Araugo OE, Flowers FP, Brown K. DICP. 1991 Jul-Aug;25(7-8):835-9.
Department of Pharmacy Practice, College of Pharmacy, University of Florida, Gainesville.

The use of vitamin D3 in the treatment of psoriasis is discussed with emphasis on positive and negative results of many clinical trials. Investigations indicate the treatment with topical vitamin D3 provides consistently more rapid clinical improvement than its oral counterpart, with no reported adverse effects. Studies have shown that 68 of 83 patients exhibited significant improvement of their psoriatic lesions with the topical application of vitamin D3 analogs, including 1,24-dihydroxycholecalciferol, calcitriol, and MC 903.

Clinical trials involving 35 patients treated with oral vitamin D3 analogs resulted in moderate improvement in 24 of the patients. Adverse effects can be minimized by bedtime dosing and possibly the use of new noncalciotropic analogs. Vitamin D3 analogs appear to provide one more promising treatment option for psoriasis.

Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to enhance antiangiogenic effects of EGCG through activation of FOXO transcription factor.

Shankar S, Chen Q, Srivastava RK.

Department of Biochemistry, University of Texas Health Science Center at Tyler, Tyler, Texas, 75708-3154, USA. rakesh.srivastava@uthct.edu. J Mol Signal. 2008 Mar 20;3:7

BACKGROUND: We have recently shown that epigallocatechin-3-gallate (EGCG), a polyphenolic compound from green tea, inhibits angiogenesis. However, the molecular mechanisms by which EGCG inhibits angiogenesis have never been investigated. In this study, we examined the interaction of PI3K/AKT and MEK/ERK pathways on the regulation of FOXO transcription factors, which ultimately control the antiangiogenic effects of EGCG.

RESULTS: Inhibition of PI3K/AKT and MEK/ERK pathways interact synergistically to inhibit migration and capillary tube formation of HUVEC cells and further enhanced the antiangiogenic effects of EGCG. Inhibition of AKT and MEK kinases synergistically induced FOXO transcriptional activity, which was further enhanced in the presence of EGCG. Phosphorylation deficient mutants of FOXO induced FOXO transcriptional activity, inhibited HUVEC cell migration and capillary tube formation. Inhibition of FOXO phosphorylation also enhanced antiangiogenic effects of EGCG through transcriptional activation of FOXO.

CONCLUSION: Inhibition of PI3K/AKT and MEK/ERK pathways act synergistically to regulate antiangiogenic effects of EGCG through activation of FOXO transcription factors. The activation of FOXO transcription factors through inhibition of these two pathways may have physiological significance in management of diabetic retinopathy, rheumatoid arthritis, psoriasis, cardiovascular diseases, and cancer.