Nuclear factor erythroid-derived 2-like 2 (Nrf-2) is transcription factor implicated in the antioxidant response element-mediated induction of endogenous antioxidant enzyme such as heme oxygenase-1 (HO-1), glutamate-cysteine ligase, and NAD(P)H quinone dehydrogenase 1, among which HO-1 is an enzyme catalyzing the degradation of heme.producing biliverdin, ferrous iron, and carbon monoxide. In the stomach, as much as regulating gastric acid secretions, well-coordinated establishment of defense system stands for maintaining gastric integrity. In previous study, author et al. for the first time discovered HO-1 induction was critical in affording faithful gastric defense against various irritants including Helicobacter pylori infection, stress, alcohol, non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, and toxic bile acids. In this review article, we can add the novel evidence that dietary walnut intake can be reliable way to rescue from NSAIDs-induced gastrointestinal damages via the induction of HO-1 transcribed with Nrf-2 through specific inactivation of Keap-1. From molecular exploration to translational animal model of indomethacin-induced gastrointestinal damages, significant induction of HO-1 contributed to rescuing from damages. In addition to HO-1 induction action relevant to walnut, we added the description the general actions of walnut extracts or dietary intake of walnut regarding cytoprotection and why we have focused on to NSAID damages.

核因子类胡萝卜素衍生的2样2（Nrf-2）是转录因子，涉及抗氧化剂响应元件介导的内源性抗氧化酶如血红素加氧酶-1（HO-1），谷氨酸半胱氨酸连接酶和NAD（ P）H醌脱氢酶1，其中HO-1是催化产生血红素的联肝素，亚铁和一氧化碳降解的酶。在胃中，与调节胃酸分泌一样，协调一致的防御系统的建立也代表着维持胃的完整性。在先前的研究中，作者等。首次发现HO-1诱导对于忠实地抵抗各种刺激物（包括幽门螺杆菌）的胃防御至关重要感染，压力，酒精，非甾体抗炎药（NSAID），阿司匹林和有毒胆汁酸。在这篇评论文章中，我们可以添加新的证据，即饮食核桃的摄入可以通过Keap-1的特异性失活诱导Nrf-2转录的HO-1来挽救NSAIDs诱导的胃肠道损害。从分子探索到吲哚美辛诱导的胃肠道损伤的转化动物模型，HO-1的大量诱导有助于挽救损伤。除了与核桃相关的HO-1诱导作用外，我们还添加了核桃提取物或核桃饮食在细胞保护方面的一般作用以及为什么我们关注NSAID损害的原因的描述。