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

作者：Meng, Xianshe; Zheng, Shihong; Yin, Zequn; Wang, Xuerui; Yang, Daigang; Zou, Tingfeng; Li, Huaxin; Chen, Yuanli; Liao, Chenzhong^*; Xie, Zhouling; Fan, Xiaodong; Han, Jihong; Duan, Yajun^*; Yang, Xiaoxiao^*

来源：Food Science and Human Wellness, 2024, 13(1): 211-224.

DOI：10.26599/FSHW.2022.9250018

• Psoriasis
• Apigenin
• Imiquimod
• Inflammation
• Signal transducer activator of transcription 3
• (STAT3)
• Nuclear factor-KB (NF-KB)

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, w e 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-KB (NF-KB) pathway. Furthermore, API reduced expression of inflammatory cytokines through inactivation of NF-KB. Taken together, our study demonstrates that API can ameliorate psoriasis and may be considered as a strategy for psoriasis treatment.& COPY; 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/).

• 单位
  南开大学