Evaluation of survivin and NF‐κB in psoriasis, an immunohistochemical study

Abdou, Asmaa Gaber; Hanout, Hayam Mohamed Aboelnasr

doi:10.1111/j.1600-0560.2007.00841.x

Cited by 70 publications

(50 citation statements)

References 23 publications

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“…Total expression of the proteins forming NF-κB, the heterodimer p50 and p65, may not be increased in psoriatic lesions [56], but the active phosphorylated form or nuclear expression of NF-κB is detected in 66% of psoriatic lesions and overexpressed in psoriasis compared with normal skin [57]. In addition, NF-κB function appears deregulated, in the sense that NF-κB DNA binding to the p53 k Bsite is decreased, whereas NF-κB binding to the pro-inflammatory interleukin-8 (IL-8) κB site is increased in lesional psoriatic skin compared with non-lesional psoriatic skin [58].…”

Section: Human Use Of Chondroitin Sulphatementioning

confidence: 99%

Immunomodulatory and anti‐inflammatory effects of chondroitin sulphate

Souich

Garcı́a

Vergés

et al. 2009

J Cellular Molecular Medi

174

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Chondroitin sulphate (CS) is a natural glycosaminoglycan present in the extracellular matrix and is formed by the 1–3 linkage of D-glucuronic acid to N-acetylgalactosamine. In chondrocytes, CS diminishes interleukin-1 p (IL-1p)-induced increases in p38 mitogen-activated protein kinase (p38MAPK) and signal-regulated kinase 1/2 (Erk1/2) phosphorylation, and decreases nuclear factor-KB (NF-kB) nuclear translocation and as a consequence, reduces the formation of pro-inflammatory cytokines, IL-1 p and TNF-a, and pro-inflammatory enzymes, such as phospholipase A2 (PLA2), cyclooxygenase 2 (COX-2) and nitric oxide synthase-2 (NOS-2). The mechanism of action of CS explains its beneficial effect on the cartilage, synovial membrane and subchondral bone. On the other hand, in vivo, CS given orally prevents hepatic NF-κB nuclear translocation, suggesting that systemic CS may elicit an anti-inflammatory effect in many tissues besides the articulation. There is preliminary evidence showing that in human beings, CS may be of benefit in other diseases where inflammation is an essential marker, such as psoriasis and atherosclerosis. The review of the literature suggest that CS might also be of interest for the treatment of other diseases with an inflammatory and/or autoimmune character, such as inflammatory bowel disease, degenerative diseases of the central nervous system and stroke, multiple sclerosis and other autoimmune diseases.

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Section: Human Use Of Chondroitin Sulphatementioning

confidence: 99%

Immunomodulatory and anti‐inflammatory effects of chondroitin sulphate

Souich

Garcı́a

Vergés

et al. 2009

J Cellular Molecular Medi

174

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“…The pathophysiology of psoriasis is complex and has not been completely elucidated. Current studies show that abnormal proliferation and differentiation of keratinocytes as well as prominent immune cell infiltration contribute to psoriasis development (Abdou & Hanout, 2008). Consistently, inhibition of the excessive proliferation of keratinocytes and proinflammatory responses has proved to be efficient methods for psoriasis treatment.…”

Section: Introductionmentioning

confidence: 98%

Metformin inhibits proliferation and proinflammatory cytokines of human keratinocytesin vitrovia mTOR-signaling pathway

Liu

Yang

et al. 2015

Pharmaceutical Biology

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Context: The antidiabetic drug metformin exhibits antiproliferative and pro-apoptotic effects in various cells, suggesting its potential to treat a variety of malignant and non-malignant hyperplastic diseases. Clinical studies indicate that psoriasis patients with metformin treatment have a better response than those without metformin. Objective: The present study evaluates the antiproliferative activity and anti-inflammatory responses of metformin in human keratinocytes in vitro and explores the underlying mechanisms. Materials and methods: HaCaT cells were incubated with metformin at 0, 25, 50, and 100 mM for 48 h. Antiproliferative activity was evaluated by MTT and apoptotic response was examined by flow cytometry. ELISA was used to detect IL-6, TNF-a, and VEGF protein expression. Western blot was used to investigate the expression of the mammalian target of rapamycin (mTOR) and its downstream effectors p70 ribosomal S6 kinase (p70S6K). Results: The survival rates of HaCaT cells treated with metformin at 50 mM were reduced to 75.6, 59.4, and 30.3% at 24, 48, and 72 h, respectively. The number of apoptotic HaCaT cells was significantly increased at 50 mM metformin after 48 h treatment. Metformin can exert an antiinflammatory effect by direct inhibition of IL-6, TNF-a, and VEGF. Metformin at 50 mM significantly reduced the phosphorylation of mTOR and p70S6K, by 49.0 and 62.1%, respectively. Discussion and conclusion: Metformin treatment significantly inhibited proliferation and proinflammatory responses in HaCaT cells by a mechanism associated with inhibition of the mTOR signaling pathway. The results indicate that metformin may be used as a potential therapeutic agent for psoriasis.

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“…Compared to normal skin, NF-kB was significantly overexpressed in psoriatic skin [73], and compounds that inhibit NF-kB translocation result in improvement of disease severity [74,75]. Investigators have also observed that, in the epidermis of psoriatic skin, there is an upregulation of NF-kB activity, and anti-TNF-a therapy leads to down-regulation of NF-kB [76].…”

Section: Ros-influenced Pathways In Psoriasismentioning

confidence: 95%