Xunwei Li ¹ Di Qianqian ¹ Xiaoli Li ² Xibao Zhao ¹ Han Wu ¹ Yue Xiao ¹ Haimei Tang ¹ Xucan Huang ¹ Jin Chen ¹ Shaoying Chen ¹ Yuli Gao ¹ Junbo Gao ² Weilie Xiao ² Weilin Chen ^1*

• ¹ Shenzhen University, Shenzhen, China
• ² Yunnan University, Kunming, Yunnan Province, China

Treatments of inflammatory bowel disease (IBD) are diverse, but their efficacy is limited and it is therefore urgent to find better therapies. Controlling mucosal inflammation is a must in IBD drug treatment. The occurrence of anti-tumor necrosis factor α (TNF-α) monoclonal antibodies has provided a safer and more efficacious therapy. However, this kind of treatment still faces failure in form of loss of response. β-Carboline alkaloids own an anti-inflammatory pharmacological activity. While Kumujan B contains β-Carboline, its biological activity still remains unknown. Our data show that Kumujan B attenuated the expression of interleukin 1β (IL-1β) and interleukin 6 (IL-6) induced by TNF-α in mouse peritoneal macrophages. Kumujan B suppressed c-Jun N-terminal protein kinases (JNK) signaling, especially c-Jun for anti-inflammatory response. Furthermore, Kumujan B promoted K11-linked ubiquitination and degradation of c-Jun through the proteasome pathway. In an in vivo study, Kumujan B inhibited the expression of IL-1β, IL-6 and TNF-α and improved the colon barrier function in dextran sulfate sodium salt (DSS)-induced experimental mice colitis. Taken together, Kumujan B exhibited anti-inflammatory effects both in vivo and vitro, which might be a potential therapeutic candidate in treating IBD.