Gallic Acid Alleviates Psoriasis Keratinization and Inflammation by Regulating BRD4 Expression
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
38830123
DOI
10.14712/fb2024070010053
PII: fb_2024070010053
Knihovny.cz E-resources
- Keywords
- BRD4, gallic acid, hyperproliferation, inflammation, keratinocytes, psoriasis,
- MeSH
- Apoptosis * drug effects MeSH
- HaCaT Cells MeSH
- Cell Line MeSH
- Adult MeSH
- Interleukin-17 metabolism MeSH
- Nuclear Proteins metabolism genetics MeSH
- Keratinocytes * drug effects metabolism MeSH
- Gallic Acid * pharmacology MeSH
- Humans MeSH
- MicroRNAs genetics metabolism MeSH
- Cell Movement * drug effects MeSH
- Cell Proliferation * drug effects MeSH
- Cell Cycle Proteins * metabolism genetics MeSH
- Bromodomain Containing Proteins MeSH
- Psoriasis * metabolism pathology drug therapy MeSH
- Gene Expression Regulation drug effects MeSH
- Transcription Factors * metabolism MeSH
- Inflammation * pathology MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- BRD4 protein, human MeSH Browser
- Interleukin-17 MeSH
- Nuclear Proteins MeSH
- Gallic Acid * MeSH
- MicroRNAs MeSH
- Cell Cycle Proteins * MeSH
- Bromodomain Containing Proteins MeSH
- Transcription Factors * MeSH
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.
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