Expression of Intercellular Adhesion Molecule - l ( ICAM - 1 ) in Vascular Endothelium and Keratinocytes of Psoriatic Skin

Ban, Dea-Hyun; Koo, Sang-Wahn; Kim, Young-Keun; Choi, Gwang‐Seong; Lee, Joo Heung

doi:10.5021/ad.2000.12.4.259

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“…The expressions of IP-10/CXCL10 and MIP-3α/CCL20, which are chemoattractants for Th1 and Th17 cells, also increased in psoriatic keratinocytes [6,48,49]. ICAM-1 is an important adhesion molecule for T-cell recruitment in psoriatic skin lesions, and the overexpression of ICAM-1 was observed in epidermal keratinocytes from psoriasis patients [50]. In the current study, the levels of IL-6, IP-10/CXCL10, MIP-3α/CCL20, and ICAM-1 were upregulated in M5-stimulated HaCaT cells (in vitro model of psoriasis).…”

Section: Discussionmentioning

confidence: 93%

Coptisine Alleviates Imiquimod-Induced Psoriasis-like Skin Lesions and Anxiety-like Behavior in Mice

et al. 2022

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Psoriasis is a common inflammatory skin disorder, which can be associated with psychological disorders, such as anxiety and depression. This study investigated the efficacy and the mechanism of action of a natural compound coptisine using imiquimod (IMQ)-induced psoriasis mice. Coptisine reduced the severity of psoriasis-like skin lesions, decreased epidermal hyperplasia and the levels of inflammatory cytokines TNF-α, IL-17, and IL-22. Furthermore, coptisine improved IMQ-induced anxiety in mice by increasing the number of entries and time in open arms in the elevated plus maze (EPM) test. Coptisine also lowered the levels of inflammatory cytokines TNF-α and IL-1β in the prefrontal cortex of psoriasis mice. HaCaT keratinocytes and BV2 microglial cells were used to investigate the effects of coptisine in vitro. In M5-treated HaCaT cells, coptisine decreased the production of IL-6, MIP-3α/CCL20, IP-10/CXCL10, and ICAM-1 and suppressed the NF-κB signaling pathway. In LPS-stimulated BV2 cells, coptisine reduced the secretion of TNF-α and IL-1β. These findings suggest that coptisine might be a potential candidate for psoriasis treatment by improving both disease severity and psychological comorbidities.

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