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Updated: Jun 24, 2025
11:39
The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
Published on: July 11, 2013
38.9K
Gallic Acid Alleviates Psoriasis Keratinization and Inflammation by Regulating BRD4 Expression
Li Zhang1, Qiaoyuan Ye2, Saiyang Gan1
1Dermatology Department, ShenZhen Qianhai Shekou Free Trade Zone Hospital, China.
Folia Biologica
|June 3, 2024
Summary
Gallic acid, a natural compound, shows promise in treating psoriasis by reducing inflammation and cell proliferation. It works by down-regulating bromodomain-containing protein 4 (BRD4) in skin cells, offering a potential new therapeutic avenue for this chronic autoimmune disease.
Area of Science:
- Dermatology
- Immunology
- Pharmacology
Background:
- Psoriasis is a chronic autoimmune skin condition.
- Gallic acid possesses various beneficial properties, but its effect on psoriasis is unclear.
- Bromodomain-containing protein 4 (BRD4) is implicated in inflammatory processes.
Purpose of the Study:
- To investigate the therapeutic effect of gallic acid on psoriasis.
- To explore the role of BRD4 in psoriatic keratinocytes.
- To determine the mechanism by which gallic acid influences psoriatic skin cells.
Main Methods:
- Collected psoriatic and healthy human skin tissues.
- Utilized human keratinocytes (HaCaT cells) treated with IL-17A to model psoriasis.
- Assessed BRD4 expression via qRT-PCR and Western blotting.
- Evaluated cell migration, proliferation, apoptosis, and inflammatory cytokine levels (IFN-γ, IL-6, IL-8, IL-17).
Main Results:
- BRD4 was upregulated in psoriatic tissues and IL-17A-treated cells.
- BRD4 silencing inhibited proliferation, migration, and inflammation while promoting apoptosis.
- Gallic acid treatment downregulated BRD4, suppressed cell migration, proliferation, and inflammation, and induced apoptosis in IL-17A-treated HaCaT cells.
Conclusions:
- BRD4 plays a significant role in the pathogenesis of psoriasis.
- Gallic acid demonstrates potential as a therapeutic agent for psoriasis.
- Gallic acid exerts its therapeutic effects by downregulating BRD4, thereby modulating keratinocyte behavior and inflammatory responses.
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