Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB

Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB

Psoriasis is a chronic autoimmune disease featured by patches on the skin. It is caused by malfunction of immune cells and keratinocytes with inflammation as one of its key features. Apigenin (API) is a natural flavonoid with anti-inflammatory and immunoregulatory properties. Therefore, we speculate...

Full description

Saved in:
Bibliographic Details
Main Authors: Xianshe Meng, Shihong Zheng, Zequn Yin, Xuerui Wang, Daigang Yang, Tingfeng Zou, Huaxin Li, Yuanli Chen, Chenzhong Liao, Zhouling Xie, Xiaodong Fan, Jihong Han, Yajun Duan, Xiaoxiao Yang
Format: Article
Language:English
Published: Tsinghua University Press 2024-01-01
Series:Food Science and Human Wellness
Subjects:
Psoriasis
Apigenin
Imiquimod
Inflammation
Signal transducer activator of transcription 3 (STAT3)
Nuclear factor-κB (NF-κB)
Online Access:http://www.sciencedirect.com/science/article/pii/S2213453023001118
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Psoriasis is a chronic autoimmune disease featured by patches on the skin. It is caused by malfunction of immune cells and keratinocytes with inflammation as one of its key features. Apigenin (API) is a natural flavonoid with anti-inflammatory and immunoregulatory properties. Therefore, we speculated that API can ameliorate psoriasis, and determined its effect on the development of psoriasis by using imiquimod (IMQ)-induced psoriasis mouse model. Our results showed that API attenuated IMQ-induced phenotypic changes, such as erythema, scaling and epidermal thickening, and improved splenic hyperplasia. Abnormal differentiation of immune cells was restored in API-treated mice. Mechanistically, we revealed that API is a key regulator of signal transducer activator of transcription 3 (STAT3). API regulated immune responses by reducing interleukin-23 (IL-23)/STAT3/IL-17A axis. Moreover, it suppressed IMQ-caused cell hyperproliferation by inactivating STAT3 through regulation of extracellular signal-regulated kinase 1/2 and nuclear factor-κB (NF-κB) pathway. Furthermore, API reduced expression of inflammatory cytokines through inactivation of NF-κB. Taken together, our study demonstrates that API can ameliorate psoriasis and may be considered as a strategy for psoriasis treatment.
ISSN:2213-4530

Similar Items