@article{Meng2024, 
author = {Xianshe Meng and Shihong Zheng and Zequn Yin and Xuerui Wang and Daigang Yang and Tingfeng Zou and Huaxin Li and Yuanli Chen and Chenzhong Liao and Zhouling Xie and Xiaodong Fan and Jihong Han and Yajun Duan and Xiaoxiao Yang},
title = {Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB},
year = {2024},
journal = {Food Science and Human Wellness},
volume = {13},
number = {1},
pages = {211-224},
keywords = {Inflammation, Psoriasis, Apigenin, Imiquimod, Signal transducer activator of transcription 3 (STAT3), Nuclear factor-κB (NF-κB)},
url = {https://www.sciopen.com/article/10.26599/FSHW.2022.9250018},
doi = {10.26599/FSHW.2022.9250018},
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.}
}