Oroxylin A suppress LL-37 generated rosacea-like skin inflammation through the modulation of SIRT3-SOD2-NF-κB signaling pathway.
Feng. Chunmei C; Zhang. Haiyan H; Wang. Peiru P; Zhang. Linglin L; Liu. Xiaojing X; Yan. Guorong G; Yan. Yu Y; Yang. Jin J; Liu. Jia J; Tan. Fei F; Wang. Xiuli X; Zeng. Qingyu Q
Key Findings
- Oroxylin A reduced rosacea‑like skin lesions and immune cell infiltration in experimental models
- It suppressed ROS production triggered by LL‑37 via the SIRT3‑SOD2 signaling pathway
- The compound inhibited activation of the NF‑κB inflammatory pathway
Practical Outcomes
- Oroxylin A could become a topical option for managing rosacea or similar skin inflammation, but the study doesn’t provide dosing guidelines or safety data for self‑use. Enthusiasts should wait for clinical trials or formulation details before trying it themselves.
Summary
A study found that Oroxylin A, a compound from traditional Chinese medicine, can lessen skin inflammation similar to rosacea caused by the peptide LL‑37. It works by lowering harmful reactive oxygen species and blocking a key inflammation pathway (NF‑κB) through the SIRT3‑SOD2 system. While the results are promising, they come from lab experiments and don’t give clear dosage or formulation advice for everyday use.
Abstract
Rosacea is a long-term inflammatory skin disease associated with the dysfunction of vascular and immunological systems. Treatment options for rosacea are difficult to implement. Oroxylin A(OA), a traditional Chinese medicine, has anti-inflammation effects in a variety of inflammatory diseases. However, it is not known that whether OA exerts protective effects against LL-37-induced rosacea. In this study, bioinformatics analyses showed that the mechanisms of rosacea and the pharmacological targets of OA were highly overlapped. Subsequently, it was shown that the administration of OA resulted in a notable amelioration of rosacea-like skin lesions, as evidenced by a reduction in immune cell infiltration, modulation of cytokine production, and inhibition of angiogenesis. Plus, it was shown that OA effectively suppressed the generation of ROS generated by LL-37, as well as the subsequent activation of NF-κB signaling pathway. To explore further, we found that OA inhibited LL-37-induced ROS production via SIRT3-SOD2 signaling pathway in keratinocytes. Based on the aforementioned evidence, it can be inferred that OA exhibits a mitigating effect on the inflammatory response in rosacea by modulating the SIRT3-SOD2-NF-κB signaling pathway.
Study Information
pubmed
2024
2024-02-15T00:00:00.000Z
10.1016/j.intimp.2024.111636
6
47