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...
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Tsinghua University Press
2024-01-01
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| Series: | Food Science and Human Wellness |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213453023001118 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Xianshe Meng |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-6988ac0544fe4466a96a186760f1e7ce |
| institution | Kabale University |
| issn | 2213-4530 |
| language | English |
| publishDate | 2024-01-01 |
| publisher | Tsinghua University Press |
| record_format | Article |
| series | Food Science and Human Wellness |
| spelling | doaj-art-6988ac0544fe4466a96a186760f1e7ce2025-02-03T02:51:42ZengTsinghua University PressFood Science and Human Wellness2213-45302024-01-01131211224Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κBXianshe Meng0Shihong Zheng1Zequn Yin2Xuerui Wang3Daigang Yang4Tingfeng Zou5Huaxin Li6Yuanli Chen7Chenzhong Liao8Zhouling Xie9Xiaodong Fan10Jihong Han11Yajun Duan12Xiaoxiao Yang13Key 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, ChinaKey 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, ChinaKey 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, ChinaKey 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, ChinaKey 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, ChinaKey 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, ChinaKey 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, ChinaKey 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, ChinaKey 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; Corresponding author at: College of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, ChinaKey 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, ChinaTianjin Key Laboratory of human Development and Reproductive Regulation, Department of General Gynecology, Tianjin Central Hospital of Gynecology and Obstetrics, Tianjin 300100, ChinaKey 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; Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials of Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, ChinaKey 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; Corresponding author at: College of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, ChinaKey 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; Corresponding author at: College of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, ChinaPsoriasis 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.http://www.sciencedirect.com/science/article/pii/S2213453023001118PsoriasisApigeninImiquimodInflammationSignal transducer activator of transcription 3 (STAT3)Nuclear factor-κB (NF-κB) |
| spellingShingle | 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 Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB Food Science and Human Wellness Psoriasis Apigenin Imiquimod Inflammation Signal transducer activator of transcription 3 (STAT3) Nuclear factor-κB (NF-κB) |
| title | Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB |
| title_full | Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB |
| title_fullStr | Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB |
| title_full_unstemmed | Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB |
| title_short | Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB |
| title_sort | apigenin ameliorates imiquimod induced psoriasis in c57bl 6j mice by inactivating stat3 and nf κb |
| topic | Psoriasis Apigenin Imiquimod Inflammation Signal transducer activator of transcription 3 (STAT3) Nuclear factor-κB (NF-κB) |
| url | http://www.sciencedirect.com/science/article/pii/S2213453023001118 |
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