Nrf2 (nuclear factor erythroid 2-related factor 2) is a stress-responsive transcription factor, associated with cellular homeostasis. Under normal conditions Nrf2 is kept in the cytoplasm by Kelch-like ECH-associated protein 1 (Keap1) which facilitates its degradation. Meanwhile, oxidative or electrophilic stress trigger Keap1 dissociation from the Nrf2/Keap1 complex and Nrf2 translocation to the nucleus where it induces the expression of numerous anti-oxidative and anti-inflammatory genes. The Nrf2/Keap1 axis plays a crucial role in the development of gastrointestinal (GI) tract and the maintenance of its proper functionality. This axis also seems to be a promising candidate for prevention of inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), as well as their severe complications such as intestinal fibrosis and colorectal cancer. This review focuses on the role of Nrf2/Keap1 in 1) the development and proper functionality of GI tract, 2) the pathophysiology of GI diseases and their long-term complications, 3) the effectiveness of currently used drugs and non-conventional treatments which influence Nrf2/Keap1 and are potentially effective in IBD treatment, as well as 4) the effect of gut microbiota on Nrf2/Keap1 pathway in IBD.

Nrf2（核因子红细胞 2 相关因子 2）是一种应激反应性转录因子，与细胞稳态相关。在正常条件下，Nrf2 被 Kelch 样 ECH 相关蛋白 1 (Keap1) 保留在细胞质中，这有助于其降解。同时，氧化或亲电应激触发 Keap1 从 Nrf2/Keap1 复合物解离和 Nrf2 易位到细胞核，在那里它诱导许多抗氧化和抗炎基因的表达。Nrf2/Keap1 轴在胃肠 (GI) 道的发育及其正常功能的维持中起着至关重要的作用。该轴似乎也是预防炎症性肠病 (IBD) 的有希望的候选者，包括溃疡性结肠炎 (UC) 和克罗恩病 (CD)，以及它们的严重并发症，如肠道纤维化和结直肠癌。本综述重点关注 Nrf2/Keap1 在 1) 胃肠道的发育和正常功能，2) 胃肠疾病的病理生理学及其长期并发症，3) 目前使用的药物和非常规治疗的有效性影响 Nrf2/Keap1 并可能对 IBD 治疗有效，以及 4) 肠道微生物群对 IBD 中 Nrf2/Keap1 通路的影响。