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Open Access

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

Xianshe Menga,1Shihong Zhenga,1Zequn Yina,Xuerui WangaDaigang YangaTingfeng ZouaHuaxin LiaYuanli ChenaChenzhong Liaoa( )Zhouling XieaXiaodong FanbJihong Hana,cYajun Duana( )Xiaoxiao Yanga( )
Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, College of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, China
Tianjin Key Laboratory of human Development and Reproductive Regulation, Department of General Gynecology, Tianjin Central Hospital of Gynecology and Obstetrics, Tianjin 300100, China
Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials of Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China

1 These authors contributed equally to this work.

Peer review under responsibility of Tsinghua University Press.

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Highlights

• Apigenin improves IMQ-induced psoriasis in C57BL/6J mice;

• Apigenin prevents IMQ-induced abnormal immune activation through inhibiting IL23/STAT3/IL17A signaling axis;

• Apigenin reduces IMQ-induced inflammation by inactivation of NF-kB;

• Apigenin inhibits cell hyperproliferation via decreasing ERK1/2 activity.

Graphical Abstract

Abstract

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.

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Food Science and Human Wellness
Pages 211-224
Cite this article:
Meng X, Zheng S, Yin Z, et al. Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB. Food Science and Human Wellness, 2024, 13(1): 211-224. https://doi.org/10.26599/FSHW.2022.9250018

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Received: 28 January 2022
Revised: 14 April 2022
Accepted: 19 May 2022
Published: 01 June 2023
© 2024 Beijing Academy of Food Sciences. Publishing services by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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