An integrated network pharmacology and molecular docking approach to reveal the role of Arctigenin against Cutibacterium acnes‐induced skin inflammation by targeting the CYP19A1

Author:

Lu Xiaoyan12ORCID,Han Yanzhong12,Zhang Yongkang3,Li Rui12,Xu Jiaoyan12,Yang Jian12,Yao Jingchun12,Lv Zhihai4

Affiliation:

1. State Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine Linyi People's Republic of China

2. National Engineering and Technology Research Center of Chirality Pharmaceutical Linyi People's Republic of China

3. College of Pharmacy Shandong University of Traditional Chinese Medicine Jinan People's Republic of China

4. Longgang District Maternity and Child Healthcare Hospital of Shenzhen City Shenzhen People's Republic of China

Abstract

AbstractAcne caused by inflammation of hair follicles and sebaceous glands is a common chronic skin disease. Arctigenin (ATG) is an extract of Arctium lappa L., which has significant anti‐inflammatory effects. However, the effect and mechanism of ATG in cutaneous inflammation mediated by Cutibacterium acnes (C. acnes) has not been fully evaluated. The purpose of this study was to explore the effect and potential mechanism of ATG in the treatment of acne through network pharmacology and experimental confirmation. An acne model was established by injected live C. acnes into living mice and treated with ATG. Our data showed that ATG effectively improved acne induced by live C. acnes, which was confirmed by determining ear swelling rate, estradiol concentration and hematoxylin and eosin (H&E) staining. In addition, ATG inhibited the NLRP3 inflammasome signaling pathway in mice ear tissues and reduced the secretion of pro‐inflammatory cytokines IL‐1β to relieve inflammation. The results of network pharmacology and molecular docking confirmed that ATG can regulate 17β‐Estradiol (E2) levels through targeted to CYP19A1, and finally inhibited skin inflammation. Taken together, our results confirmed that ATG regulated E2 secretion by targeting CYP19A1, thereby inhibiting the NLRP3 inflammasome signaling pathway and improving inflammation levels in acne mice. This study provides a basis for the feasibility of ATG in treating acne in clinical practice.

Funder

Natural Science Foundation of Shandong Province

Publisher

Wiley

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