Skip to main content
You're viewing the free public version. Create a free account for full research and member tools. Join free
Research Abstract Animal Study

Gallic acid alleviates psoriasis keratinization and inflammation by regulating BRD4 expression.

Gallic Acid Alleviates Psoriasis Keratinization and Inflammation by Regulating BRD4 Expression.

0:00 / 0:00
0:00 / 0:00

Sign in to access this feature

Create a free account or sign in to use AI summaries, listen to articles, download PDFs, and save to your library.

90 views
Share:

Abstract

Psoriasis is a chronic non-contagious autoimmune disease. Gallic acid is a natural compound with potential health benefits, including antioxidant, anticancer, antiviral and antibacterial properties. Nevertheless, the influence of gallic acid on psoriasis has not been fully determined. This investigation aimed to discover the effect of gallic acid on psoriasis. Thirty-one pairs of psoriatic skin tissues and healthy adult human skin tissues were collected. Human keratinocytes (HaCaT cells) were transfected with interleukin 17A (IL-17A) to create the psoriatic keratinocyte model. The content of bromodomain-containing protein 4 (BRD4) microRNA was assessed using qRT-PCR testing. The content of BRD4 was detected by Western blotting. Cell migration was evaluated by conducting a wound healing assay. Cell proliferation was determined using an EdU assay. Apoptosis was detected by the TUNEL assay. The contents of interferon gamma (IFN-γ), IL-6, IL-8 and IL-17 were detected by ELISA. BRD4 was up-regulated in psoriatic skin tissues and in the IL-17A group compared to the healthy adult human skin tissues and the control group. Silencing BRD4 inhibited cell migration, proliferation and inflammatory response but induced apoptosis in IL-17A-treated HaCaT cells. Conversely, BRD4 over-expression promoted cell migration, proliferation and inflammatory response but suppressed apoptosis in IL-17A-treated HaCaT cells. Gallic acid repressed cell migration, proliferation and inflammatory response but indu-ced apoptosis in HaCaT cells transfected with IL-17A by down-regulating BRD4. Gallic acid represses cell migration, proliferation and inflammatory response but induces apoptosis in IL-17A-transfected HaCaT cells by down-regulating BRD4.

Affiliation

Li Zhang

External References

PubMed ID:
38830123

Comments

Sign in or create a free account to join the conversation.

Sign in to comment

Be the first to comment.

More Research Abstracts

View All Abstracts
Animal Study

Findings highlight the therapeutic potential of these compounds in mitigating tissue damage and inflammation associated with ovarian transplant.

Aug 31, 2024 Papatya Keles, Tansel Sapmaz, Kubra Basol Baki, Sude Topkaraoglu, Esra Erdem, Kubra Sevgin, Sibel Kuras, Mahmud Esad Pence, Selman Aktas, Burak Karip

Exp Clin Transplant

Trusted By Professionals and Teams:

The National Health Federation
Stand For Health Freedom
Global Healing Institute
Global Wellness Forum
MAHA Action
Myers Detox
Natural News
Mercola.com

Unlock Evidence-Based Health Research

Join 500,000+ members accessing 10,000+ natural health topics.

Subscribe to our informative Newsletter & Receive

Cancer Fighting Foods Ebook

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.