Menu
Peptide Database
Results
No peptides found
Featured

Use search to browse all 100+ peptides

LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 2
2024 pubmed 2 citations

Tranilast alleviates skin inflammation and fibrosis in rosacea-like mice induced by long-term exposure to LL-37.

Jin. Hui H; Wu. Yiling Y; Zhang. Chuanxi C; Zheng. Ruiping R; Xu. Hong H; Yang. Jie J; Li. Linfeng L

Key Findings

  • Tranilast lessened skin lesions and thickness in LL‑37‑induced rosacea mice
  • It decreased inflammatory cytokines (TNF‑α, IL‑6, IL‑1β, IL‑18) and the antimicrobial peptide CAMP
  • It inhibited NLRP3 inflammasome activation, TLR4 signaling, and the TGF‑β1/Smad2/3 fibrosis pathway

Practical Outcomes

  • Tranilast appears promising for reducing rosacea‑related inflammation and fibrosis in animal models, but human data are lacking. Biohackers should view this as early‑stage evidence and await clinical trials before considering off‑label use, and any experimentation should be done with medical supervision.

Summary

In a mouse study, the drug tranilast reduced skin redness, swelling, and scarring caused by the peptide LL‑37, which mimics rosacea. It lowered several inflammation signals and blocked pathways that lead to skin fibrosis, suggesting it could help treat rosacea symptoms.

Abstract

Rosacea, a prevalent chronic facial inflammatory condition, afflicts millions worldwide. Its multifaceted pathogenesis poses challenges for effective treatment. Tranilast (TR), an analog of a tryptophan metabolite, has demonstrated anti-inflammatory and anti-fibrotic properties across various diseases. Yet, its potential in rosacea treatment remains understudied. Here, we induced rosacea-like symptoms in mice via prolonged LL-37 injections and administered TR intervention. Our findings reveal that TR mitigated skin lesions, reduced skin thickness, and suppressed inflammatory cell infiltration within the dermis of LL-37 mice. Notably, TR downregulated the expression of rosacea-associated inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) and the antimicrobial peptide CAMP, while also inhibiting NLRP3 inflammasome activation and the TLR4 signaling pathway. Furthermore, TR attenuated LL-37-induced fibrosis and hindered the transforming growth factor-β1 (TGF-β1)/Smad2/3 pathway. In summary, our study underscores TR's therapeutic potential in rosacea by mitigating both skin inflammation and fibrosis, thereby offering a promising treatment avenue for this condition.

Study Information

Provider

pubmed

Year

2024

Date

2024-08-08T00:00:00.000Z

DOI

10.1016/j.bbrc.2024.150523

Citations

2

References

36