Apigenin inhibits colonic inflammation and tumorigenesis by suppressing STAT3-NF-κB signaling

// Xiao-Yu Ai 1, * , Yuan Qin 1, 2, * , Hui-Jua Liu 2, * , Zhan-Hong Cui 1, 2 , Meng Li 1, 2 , Jia-Huan Yang 1, 2 , Wei-Long Zhong 1, 2 , Yan-Rong Liu 2 , Shuang Chen 2 , Tao Sun 1, 2 , Hong-Gang Zhou 1, 2 and Cheng Yang 1, 2 1 State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China 2 Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China * These authors have contributed equally to this work Correspondence to: Cheng Yang, email: Cheng.yang@nankai.edu.cn Hong-Gang Zhou, email: honggang.zhou@vip.126.com Keywords: apigenin; IBD; CAC; NF-κB; STAT3 Received: July 04, 2017      Accepted: August 17, 2017      Published: October 27, 2017 ABSTRACT 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.