Oxymatrine protects against DSS-induced colitis via inhibiting the PI3K/AKT signaling pathway

Publication date: December 2017
Source:International Immunopharmacology, Volume 53
Author(s): Qianyun Chen, Xueyun Duan, Heng Fan, Meng Xu, Qing Tang, Lijuan Zhang, Zhexing Shou, Xingxing Liu, Dongmei Zuo, Jia Yang, Shuangjiao Deng, Yalan Dong, Hui Wu, Yujin Liu, Zhen Nan
Oxymatrine (OMT), an alkaloid derived from the root of the Sophora flavescens, has been reported to possess a significant effect on relieving UC owing to its anti-inflammatory property. But the other therapeutic mechanism of OMT remains unclear. Recent studies have found, PI3K/AKT signaling pathway is involved in the pathogenesis of UC by pro-inflammatory effects and activating T cells. Moreover, PI3K/AKT pathway is one of the most important pathways for regulating cell apoptosis. Thus, we aim to explore whether OMT protects against UC by targeting PI3K/AKT pathway. We established the UC mice models, using LY294002 (a specific inhibitor of PI3K/AKT) as a positive control, to observe the effect of low, medium and high dose of OMT on UC and its influence on PI3K/AKT signaling pathway. Our data indicated that OMT can significantly ameliorate UC through anti-inflammatory, pro-apoptotic, down-regulating the differentiation of Th1 and Th17 cells via PI3K/AKT pathway. This study reveals that PI3K/AKT signaling pathway is a potential mechanism of OMT-induced UC remission and suggests that OMT is a promising therapeutic agent for the treatment of UC.

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