Ask about this productRelated genes to: NQO1 antibody
- 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 antibody
Related articles to: NQO1 antibody
- To investigate the protective role and underlying mechanisms of Myricetin (Myr) in lipopolysaccharide (LPS)-induced acute lung injury (ALI), with emphasis on its modulation of oxidative stress and pyroptosis. - Source: PubMed
Publication date: 2026/05/16
Cao JingJia ZaixingHe KunSong BeibeiChao LingshanWang BoliQi QianChen ZixiaoXu Haibo - Ferroptosis is an iron-dependent programmed cell death modality characterized by the massive accumulation of lipid peroxides (LPO). However, the efficiency of ferroptosis is commonly limited by insufficient supply of iron ions and endogenous hydrogen peroxide (HO) in the tumor cells. To overcome these drawbacks, MIL-100 NPs were synthesized via a microwave-assisted method to encapsulate β-lapachone (Lap), followed with the hyaluronic acid (HA) surface modification (designated as LMH NPs). LMH NPs exhibited GSH-responsive degradation in the tumor cells to release Lap and Fe. The released of Lap could generate HO via catalysis by tumor-overexpressed quinone oxidoreductase 1 (NQO1), leading to increased intracellular HO levels. The abundant production of HO could supply substrates for Fe-mediated Fenton reactions to produce toxic hydroxyl radicals (·OH), thereby promoting LPO accumulation and enhancing ferroptosis. Meanwhile, Fe⁺ released from LMH NPs was reduced to Fe through GSH consumption, which could diminish glutathione peroxidase 4 (GPX4) activity. In vitro and in vivo experiments confirmed that LMH NPs possessed effective targeted uptake and exhibited optimal tumor inhibition without significant toxic side effects. Overall, the integrated strategy presents a novel ferroptosis-based clinical approach for enhanced breast cancer therapy. - Source: PubMed
Publication date: 2026/05/15
He ChudongZhao YuanyuanMo MengdieSu YuhongQi ZhongquanChen Xiao DongZhou WeijieYu Fei - This study investigated the neuroprotective effects and mechanisms of poliumoside (POL) against ischemic stroke, focusing on oxidative stress and mitochondrial dysfunction. Using an Oxygen-Glucose Deprivation/Reperfusion (OGD/R) model in Neuro-2a cells and a photothrombotic stroke model in C57BL/6J mice, we demonstrated that POL treatment significantly improved post-injury outcomes. In mice, POL enhanced motor coordination and grip strength, reduced cerebral infarct volume, and alleviated neuronal damage and apoptosis. Crucially, it suppressed brain oxidative stress, as shown by decreased reactive oxygen species (ROS) levels. In OGD/R-injured Neuro-2a cells, POL dose-dependently increased cell viability, reduced ROS and apoptosis, and improved mitochondrial function by stabilizing membrane potential and attenuating calcium overload. Mechanistically, POL activated the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway antioxidant pathway, promoting Nrf2 nuclear translocation and upregulating downstream proteins Heme oxygenase 1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1). It also modulated autophagy by affecting Microtubule-associated proteins 1A/1B light chain 3B (LC3B) and Sequestosome 1 (SQSTM1), and exerted anti-apoptotic effects by regulating B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax). In conclusion, POL confers protection against ischemic injury primarily by mitigating oxidative stress and preserving mitochondrial integrity via activation of the Nrf2 pathway and regulation of associated cellular processes. - Source: PubMed
Publication date: 2026/05/14
Qin RuiHan Bo-WenTao Jing-YingJin Xian-ZhuZhang Wen-FangZhao Wen-LeFeng Wan-DiDu Guan-HuaWang Yue-Hua - Aflatoxin B (AFB) is a common mycotoxin present in animal feed. This study systematically examined the protective effects of the novel aflatoxin oxidase CotA in alleviating the adverse impacts of AFB on broilers. A total of 432 one-day-old Arbor Acres Plus broiler chicks were randomly assigned to four experimental groups. Experimental diets consisted of a control (CON) group fed the basal diet, an AFB group supplemented with 200 μg/kg aflatoxin B, a CotA group supplemented with 5 U/kg aflatoxin oxidase CotA laccase, and a CotA+ AFB group supplemented with both 200 μg/kg aflatoxin B and 5 U/kg aflatoxin oxidase CotA. Compared with the control group, broilers exposed to AFB exhibited a 10.8 % reduction in 42-day body weight and a 13.2 % increase in the F/G ratio from 22 to 42 d (P < 0.05). Furthermore, AFB exposure significantly compromised meat quality, as evidenced by a 25.4 % increase in drip loss and an 18.4 % increase in cooking loss in the breast muscle (P < 0.05). However, these adverse effects were effectively mitigated by aflatoxin oxidase CotA supplementation, which restored the 42-day body weight to 2298.45 g and reduced the drip loss and cooking loss to 1.59 % and 35.48 %, respectively. Notably, the architectural integrity of hepatocytes in the livers of broilers fed AFB-contaminated feed was compromised, characterized by pronounced vacuolar degeneration and infiltration of inflammatory cells. The liver index in the AFB group was also significantly higher, accompanied by marked increases in serum activities of aminotransferases (ALT and AST) and alkaline phosphatase (ALP) (P < 0.05). The incorporation of aflatoxin oxidase CotA into AFB-contaminated feed effectively mitigated growth retardation and enhanced meat quality. Furthermore, compared with the AFB group, aflatoxin oxidase CotA significantly improved the hepatic activities of antioxidant enzymes, including total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) (P < 0.05). Simultaneously, dietary aflatoxin oxidase CotA supplementation effectively alleviated AFB-induced hepatic oxidative stress and ferroptosis in broilers. Mechanistically, aflatoxin oxidase CotA activated the Nrf2 signaling pathway, as demonstrated by the upregulated mRNA expression of Nrf2, NQO1, and HO-1 (P < 0.05). Regarding ferroptosis inhibition, aflatoxin oxidase CotA treatment significantly reversed AFB-induced iron overload by downregulating the expression of iron-acquisition genes (TFR1, DMT1, and STEAP3) and reduced Fe content (P < 0.05). Furthermore, aflatoxin oxidase CotA suppressed ACSL4/LPCAT3-mediated lipid peroxidation and enhanced the antioxidant system by upregulating the key ferroptosis defense genes GPX4, SLC7A11, and FSP1, leading to increased GSH levels and decreased MDA content (P < 0.05). In comparison to the AFB group, the addition of aflatoxin oxidase CotA markedly decreased the accumulation of AFB, AFBO residues, and AFB-DNA adducts in the liver (P < 0.05). Concurrently, dietary supplementation with aflatoxin oxidase CotA effectively alleviated AFB-induced intestinal villi disruption and significantly enhanced the villus height-to-crypt depth (V/C) ratio by approximately 25 % in both the jejunum and ileum (P < 0.05). Notably, aflatoxin oxidase CotA significantly preserved mucosal barrier integrity through the 1.5 to 2-fold upregulation of essential tight junction proteins. These results suggest that aflatoxin oxidase CotA holds potential as a novel feed additive to counteract the harmful impacts of AFB in broilers. - Source: PubMed
Publication date: 2026/05/02
Rao ZhiyongGuo MingluDuan XiaoyaoCao YuangeZhang WeiWang ZhixiangGuo Yongpeng - Hepatocellular carcinoma (HCC) is the predominant type of primary liver cancer. This study aimed to elucidate the involvement of genes associated with 25 cell-death modalities in HCC development and progression. HCC transcriptomic datasets were integrated with curated cell death-related genes. Candidate genes were screened by differential expression analysis and protein-protein interaction network construction. Prognostic genes were identified using univariate Cox regression, proportional hazards assumption testing, and stepwise multivariate Cox regression. A risk score model and a nomogram were established, followed by risk stratification and analyses of immune infiltration, immune checkpoints, somatic mutations, and in silico drug sensitivity. Single-cell RNA sequencing was used to identify key cell types, infer temporal dynamics, and characterize intercellular communication, and findings were validated by quantitative real-time PCR (qRT-PCR). MAPT, CDKN2A, NQO1, CHGA, SERPINE1, and RET were identified as prognostic genes, and the risk model and nomogram showed good prognostic performance. Immune profiling revealed significant differences in multiple immune cell subsets between risk groups, including activated CD4+ T cells. Notably, CDKN2A correlated with activated CD4+ T cells, NQO1 with natural killer cells, RET with CD4+ central memory cells, and SERPINE1 with activated dendritic cells; RET also showed the strongest positive correlation with HAVCR2. Mutation spectra differed across risk groups, and ten drugs displayed significant predicted IC50 differences; all six genes were negatively correlated with KIN001.135. Single-cell analyses highlighted hepatocytes as a key cell type with strong hepatocyte-epithelial communication. qRT-PCR confirmed higher MAPT, CDKN2A, NQO1, and SERPINE1 expression in HCC tissues than in normal tissues. - Source: PubMed
Publication date: 2026/04/22
Wu WeiWang YingjiZhao XiaochengDong KeLi MaodeAn XiangXu YingyanWang ShuaiLi Dexin