Ask about this productRelated genes to: NQO1 Blocking Peptide
- Gene:
- NQO1 NIH gene
- Name:
- NAD(P)H quinone dehydrogenase 1
- Previous symbol:
- NMOR1, DIA4
- Synonyms:
- DHQU, QR1, DTD
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-07-12
Related products to: NQO1 Blocking Peptide
Related articles to: NQO1 Blocking Peptide
- Follicular lymphoma (FL) remains an incurable B-cell malignancy with high relapse rates, and conventional therapies are often limited by significant toxicity, highlighting the need for novel treatments. We identified that FL exhibits markedly low expression of NAD(P)H: quinone oxidoreductase 1 (NQO1), a key enzyme required for activating quinone-based chemotherapeutics. To overcome this, we developed a novel therapeutic strategy that simultaneously upregulates NQO1 expression and provides its quinone substrate within tumor cells. This approach leverages the dual biological function of Cu , which acts as both an inducer of NQO1 expression via the Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and a catalyst for the oxidation of EGCG to its quinone form. Using a CD20-targeted nanoplatform as a delivery tool, we achieved specific co-delivery of EGCG and Cu to follicular lymphoma cells. This strategy triggered a potent NQO1-mediated redox cycle, resulting in severe NADH depletion and profound oxidative stress. These events activated the GADD45β-MAPK stress-signaling pathway, leading to mitochondrial dysfunction and apoptosis activation. In a murine FL xenograft model, this approach achieved 85% tumor growth inhibition, while maintaining a favorable safety profile. This work establishes a new therapeutic paradigm for FL, leveraging intrinsic enzyme deficiency to induce tumor-specific, self-amplifying cell death. - Source: PubMed
Publication date: 2026/05/07
Zhang JinxingWang ZiqiWeng YeFu YulinJiang YuelongZhuang BeilinZeng WenziZhang XiangchunXu BingZha JieZhuang Hongjun - While lung-protective ventilation strategies are standard care, effective adjunctive pharmacotherapies for ventilator-induced lung injury (VILI) remain lacking. Disruption of circadian (diurnal) rhythms is implicated in various lung pathologies, and the exploration of circadian regulation in VILI has emerged as a clinically relevant research direction for optimizing mechanical ventilation strategies. We hypothesized that the pulmonary Bmal1/Per2 axis confers protection against VILI by activating the Nrf2 antioxidant pathway. - Source: PubMed
Publication date: 2026/05/04
Li De-ChaoWu Ming-HuiRuan Hong-Yan - Accumulating evidence suggests that diabetes mellitus (DM) aggravates the incidence and severity of ischemia reperfusion injury (IRI). Eriodictyol (EDT), a natural flavonoid with reported nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant and anti-diabetic abilities, has been shown to mitigate IRI in various experimental models. However, its potential effect in diabetic IRI models remains unidentified. This study is aiming to explore the protective role of EDT against hyperglycemia-aggravated IRI and its underlying mechanism. - Source: PubMed
Publication date: 2026/05/05
Zhang NianlongLi XuyangYang YunlongLiu ZilinXie EnbeiZhu ZhengjieZhong YujianZhou Jianlin - Heat strokes represent a critical health issue with high mortality when severe, yet treatments are limited and do not target core pathogenic mechanisms. Oxidative stress is instrumental in heat stroke progression and is closely related to inflammatory activation and endothelial damage. Nuclear factor erythroid 2-related factor 2 (NRF2) is a key antioxidant signaling molecule in sepsis, ischemia-hypoxic encephalopathy, and trauma, although its potential role(s) in heat stroke is unknown. - Source: PubMed
Publication date: 2026/04/16
Lin GuodongGuo HaiyangYin BinglingXu ChongxiaoChen TingZhao YueliWen QiangShao YuPan Zhiguo - Weaning stress is frequently associated with intestinal oxidative stress, inflammatory activation, and epithelial apoptosis in piglets. This study investigated whether dietary supplementation with Chinese yam ( L., YAM) alleviates weaning-induced intestinal injury by modulating the oxidative stress-inflammation-apoptosis axis. 48 weaned piglets were assigned to a control diet or diets supplemented with low (1%)/high (2%) doses of YAM. Intestinal morphology, antioxidant capacity, inflammatory signaling, and apoptosis-related markers were assessed, and jejunal transcriptomic profiling was also performed. Supplementing with YAM improved villus architecture and enhanced intestinal antioxidant properties, manifested as increased total antioxidant capacity and reduced malondialdehyde levels. At the molecular level, YAM activated the Keap-1/Nrf2/HO-1 pathway and upregulated the expression of antioxidant-related genes, including superoxide dismutase 2 (SOD2), catalase (CAT), and NAD(P)H quinone dehydrogenase 1 (NQO1), and suppressed NF-κB signaling by reducing Myd88 and p-p65 protein levels. In addition, YAM modulated mitochondrial apoptosis by upregulating Bcl-2 and reducing the expression of Bax and Cleaved caspase-3. Transcriptomic analysis identified 1227 differentially expressed genes between the control and high-dose groups (784 upregulated and 443 downregulated). Mechanism-oriented module analysis further confirmed coordinated enhancement of antioxidant pathways alongside suppression of inflammatory and apoptotic gene signatures. These findings demonstrate that dietary YAM supplementation attenuates weaning-associated intestinal injury by rebalancing oxidative stress, inflammatory signaling, and apoptosis-related pathways, thereby supporting its potential application as a functional feed additive in swine production. - Source: PubMed
Publication date: 2026/04/08
Shi XiongweiGe ShaoguangWang HaiminChen XiaowangPan XiangyiLiu ChenQiu ZhengyingZou WenshuCao HaoLiu YujiaBai QiyuXin Ruihua