Apigenin inhibits colonic inflammation and tumorigenesis by suppressing STAT3-NF-κB signaling
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Xiao-Yu Ai1,*, Yuan Qin1,2,*, Hui-Jua Liu2,*, Zhan-Hong Cui1,2, Meng Li1,2, Jia-Huan Yang1,2, Wei-Long Zhong1,2, Yan-Rong Liu2, Shuang Chen2, Tao Sun1,2, Hong-Gang Zhou1,2 and Cheng Yang1,2
1State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China
2Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China
*These authors have contributed equally to this work
Cheng Yang, email: Cheng.email@example.com
Hong-Gang Zhou, email: firstname.lastname@example.org
Keywords: apigenin; IBD; CAC; NF-κB; STAT3
Received: July 04, 2017 Accepted: August 17, 2017 Published: October 27, 2017
Apigenin is a naturally occurring compound with anti-inflammatory, antioxidant, and anticancer properties. Here, we investigated the effects of apigeninin inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Apigenin effectively inhibited ulcerative colitis, a type of IBD, and CAC. Apigenin decreased myeloperoxidase (MPO), inflammatory cytokine and COX-2 levels, and it attenuated inflammatory cell infiltration in treated colon tissues as compared to untreated model colon tissues. Apigenin also reduced NF-κB and STAT3 activity in vitro and in vivo, thereby inhibiting inflammation and inflammation-induced carcinogenesis. Thus apigenin appears to inhibit inflammation and inflammation-induced carcinogenesisin IBD and CAC by suppressing STAT3-NF-κB signaling.
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