# Triticum vulgare Extract Treatment in UVB-Exposed Human Dermal Fibroblasts Modulates Inflammation, Fibrosis and Oxidative Stress Markers

**Authors:** Concetta Sozio, Stefano Caccavale, Eugenia Veronica Di Brizzi, Margherita Auriemma, Maddalena Nicoletti, Giuseppe Argenziano, Ciro Menale, Anna Balato

PMC · DOI: 10.3390/ph19020232 · Pharmaceuticals · 2026-01-29

## TL;DR

A wheat extract protects skin cells from UVB damage by reducing inflammation, fibrosis, and oxidative stress.

## Contribution

The study demonstrates the protective effects of Triticum vulgare extract in UVB-exposed fibroblasts, particularly with pretreatment.

## Key findings

- DTVE preserved cell viability and reduced UVB-induced pro-inflammatory cytokines.
- The extract limited fibroblast-to-myofibroblast transition and mitochondrial oxidative stress.
- Pretreatment with DTVE provided stronger protection than post-treatment.

## Abstract

Background/Objectives: UVB radiation triggers oxidative stress, inflammation and extracellular matrix (ECM) remodeling in dermal fibroblasts, contributing to skin aging and fibrosis. Plant-derived extracts with antioxidant and anti-inflammatory activity may counteract these effects. This study evaluated the protective role of Damor Triticum vulgare Aqueous Extract (DTVE) in human dermal fibroblasts (HDFs) exposed to UVB. Methods: Primary HDFs were irradiated with UVB (1.50 J/m2) and treated with DTVE either after irradiation (post-ir) or before and after irradiation (pre-ir). Cell viability was assessed by Trypan Blue and MTT assays. Inflammatory cytokines, fibrosis-related genes, p21 expression, mitochondrial ROS (MitoSOX) and αSMA accumulation were quantified by qRT-PCR, ELISA and immunofluorescence. Results: DTVE was not cytotoxic and preserved HDF viability under UVB exposure. UVB significantly increased pro-inflammatory cytokines, profibrotic markers, αSMA, mitochondrial ROS and p21. DTVE reduced all these UVB-induced alterations, with the pre-ir regimen providing the strongest protection. The extract attenuated early inflammatory activation, limited fibroblast-to-myofibroblast transition and decreased mitochondrial oxidative stress while reducing p21 upregulation. Conclusions: DTVE exerts protective antioxidant, anti-inflammatory and antifibrotic effects in UVB-exposed fibroblasts, particularly when used as pretreatment. These findings support DTVE as a promising candidate to mitigate UVB-induced dermal damage and warrant further investigation for potential therapeutic and cosmetic applications.

## Linked entities

- **Genes:** CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026], ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58]
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** ACTA2 (actin alpha 2, smooth muscle) [NCBI Gene 59] {aka ACTSA, SMDYS}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, SPARC (secreted protein acidic and cysteine rich) [NCBI Gene 6678] {aka BM-40, OI17, ON, ONT}, CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026] {aka CAP20, CDKN1, CIP1, MDA-6, P21, SDI1}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, JUNB (JunB proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 3726] {aka AP-1}, H3P16 (H3 histone pseudogene 16) [NCBI Gene 644914] {aka H3.6, H3F3AP6, p21}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, ELN (elastin) [NCBI Gene 2006] {aka ADCL1, SVAS, WBS, WS}, COL1A1 (collagen type I alpha 1 chain) [NCBI Gene 1277] {aka CAFYD, EDSARTH1, EDSC, OI1, OI2, OI3}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** skin damage (MESH:D012871), Inflammation (MESH:D007249), injury to (MESH:D014947), Fibrosis (MESH:D005355), cytotoxic (MESH:D064420), cutaneous damage (MESH:D045743)
- **Chemicals:** phenolic acids (MESH:C017616), CPDs (MESH:D011740), water (MESH:D014867), tetrazolium (MESH:D013778), carotenoids (MESH:D002338), MitoSOX Red (MESH:C000597839), nitric oxide (MESH:D009569), hyaluronic acid (MESH:D006820), ascorbic acid (MESH:D001205), isopropanol (MESH:D019840), P (MESH:D010758), formazan (MESH:D005562), Trypan Blue (MESH:D014343), Triton  X-100 (MESH:D017830), lipids (MESH:D008055), polyphenol (MESH:D059808), glutamine (MESH:D005973), CO2 (MESH:D002245), DAPI (MESH:C007293), DMSO (MESH:D004121), flavonoids (MESH:D005419), ROS (MESH:D017382), MitoSOX (MESH:C521281), oligosaccharide (MESH:D009844), superoxide (MESH:D013481), Dulbecco's Modified Eagle Medium (-), NO (MESH:D009614), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MESH:C022616), S (MESH:D013455), Alexa Fluor 488 (MESH:C000711379), MTT (MESH:C070243)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** HDF — Homo sapiens (Human), Induced pluripotent stem cell (CVCL_RJ31)

## Full text

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## Figures

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## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942941/full.md

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Source: https://tomesphere.com/paper/PMC12942941