<i>Coptis chinensis</i> Franch Directly Inhibits Proteolytic Activation of Kallikrein 5 and Cathelicidin Associated with Rosacea in Epidermal Keratinocytes.
Roh. Kyung-Baeg KB; Ryu. De-Hun DH; Cho. Eunae E; Weon. Jin Bae JB; Park. Deokhoon D; Kweon. Dae-Hyuk DH; Jung. Eunsun E
Key Findings
- Coptis chinensis down‑regulates KLK5 and cathelicidin expression in keratinocytes
- It directly inhibits KLK5 protease activity, preventing conversion of inactive cathelicidin to active LL‑37
- Reduced LL‑37 processing leads to lower pro‑inflammatory cytokine release
- The extract blocks TLR2 activation by Demodex chitin and downstream signaling
- It suppresses LL‑37‑induced proliferation of microvascular endothelial cells, reducing erythema
Practical Outcomes
- Using a standardized Coptis chinensis extract as a topical cream or serum could help manage rosacea by targeting the LL‑37 pathway. Biohackers can experiment with low‑dose, patch‑tested applications to assess skin tolerance and efficacy. No specific dosing is provided, so start with a small amount and monitor for irritation.
Summary
The study shows that an herbal extract from Coptis chinensis can block the skin enzymes that turn an inactive protein into the active inflammatory peptide LL‑37, which is a key driver of rosacea. By doing this, the extract also lowers inflammation signals and reduces blood‑vessel growth that cause redness. For DIY health enthusiasts, this suggests a natural, topical way to calm rosacea‑related skin flare‑ups.
Abstract
Rosacea is a common and chronic inflammatory skin disease that is characterized by dysfunction of the immune and vascular system. The excessive production and activation of kallikerin 5 (KLK5) and cathelicidin have been implicated in the pathogenesis of rosacea. <i>Coptis chinensis</i> Franch (CC) has been used as a medicinal herb in traditional oriental medicine. However, little is known about the efficacy and mechanism of action of CC in rosacea. In this study, we evaluate the effect of CC and its molecular mechanism on rosacea in human epidermal keratinocytes. CC has the capacity to downregulate the expression of KLK5 and cathelicidin, and also inhibits KLK5 protease activity, which leads to reduced processing of inactive cathelicidin into active LL-37. It was determined that CC ameliorates the expression of pro-inflammatory cytokines through the inhibition of LL-37 processing. In addition, it was confirmed that chitin, an exoskeleton of <i>Demodex</i> mites, mediates an immune response through TLR2 activation, and CC inhibits TLR2 expression and downstream signal transduction. Furthermore, CC was shown to inhibit the proliferation of human microvascular endothelial cells induced by LL-37, the cause of erythematous rosacea. These results demonstrate that CC improved rosacea by regulating the immune response and angiogenesis, and revealed its mechanism of action, indicating that CC may be a useful therapeutic agent for rosacea.
Study Information
pubmed
2020
2020-11-26T00:00:00.000Z
10.3390/molecules25235556
15
50