Cutaneous delivery of [1-(4-chloro-3-nitrobenzenesulfonyl)-1H-indol-3-yl]-methanol, an indole-3-carbinol derivative, mitigates psoriasiform lesion by blocking MAPK/NF-κB/AP-1 activation.
Clicks: 269
ID: 40078
2019
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Popular Article
75.8
/100
269 views
220 readers
Trending
AI Quality Assessment
Not analyzed
Readership in this journal
PopularRanked #28 of 39 articles by views in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
Most read
Least read
Bar heights use a square-root scale.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
[1-(4-chloro-3-nitrobenzenesulfonyl)-1H-indol-3-yl]-methanol (CIM) has been used as a bioactive agent for inhibiting tumor growth and angiogenesis via mitogen-activated protein kinase (MAPK) and NF-κB blocking. The present work was undertaken to investigate the potential of CIM against psoriasis using imiquimod (IMQ)-stimulated psoriasis-like mouse and in vitro HaCaT keratinocytes as the models. We demonstrated that topical CIM treatment reduced IMQ-activated scaling, erythema, and barrier dysfunction. This compound also restrained the recruitment of neutrophils. The cytokines, including TNF-α, IL-1β, IL-6, and IL-17 in psoriasiform skin, can be attenuated to normal baseline by CIM. Topically applied CIM can be easily delivered into skin based on the affinity with stratum corneum (SC) ceramides. IMQ intervention increased the permeability by 3-fold as compared to healthy skin. CIM ameliorated psoriatic lesion without incurring overt signs of irritation. Both TNF-α and IMQ were employed as the stimulators to activate HaCaT for reciprocal elucidation of the mechanism of action. CIM inhibited the overexpression of IL-1β, IL-6, and IL-24 in HaCaT. CIM exerted anti-inflammatory activity by suppressing the phosphorylation of NF-κB and activator protein-1 (AP-1) through MAPK pathways. Our results indicate that CIM has potential as the antipsoriatic molecule. The detailed signaling pathways still need further investigation.
| Reference Key |
weng2019cutaneousbiomedicine
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Weng, Jing-Ru;Huang, Tse-Hung;Lin, Zih-Chan;Alalaiwe, Ahmed;Fang, Jia-You; |
| Journal | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie |
| Year | 2019 |
| DOI |
S0753-3322(19)33482-1
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.