NQO1 mAb (A180)
- Known as:
- NQO1 mAb (A180)
- Catalog number:
- ASAOSA-700F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- NQO1 mAb (A180)
Related genes to: NQO1 mAb (A180)
- Gene:
- ABLIM2 NIH gene
- Name:
- actin binding LIM protein family member 2
- Previous symbol:
- -
- Synonyms:
- KIAA1808
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-19
- Date modifiied:
- 2019-03-21
- Gene:
- LRRIQ1 NIH gene
- Name:
- leucine rich repeats and IQ motif containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ12303, KIAA1801
- Chromosome:
- 12q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-01
- Date modifiied:
- 2016-10-05
- Gene:
- MAP3K21 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 21
- Previous symbol:
- -
- Synonyms:
- KIAA1804, MLK4
- Chromosome:
- 1q42.2
- Locus Type:
- gene with protein product
- Date approved:
- 2016-10-19
- Date modifiied:
- 2016-11-15
- 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
- Gene:
- ZNF333 NIH gene
- Name:
- zinc finger protein 333
- Previous symbol:
- -
- Synonyms:
- KIAA1806
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-07
- Date modifiied:
- 2015-02-26
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- Methotrexate (MTX) is a widely used chemotherapeutic and immunosuppressive agent; however, its clinical use is limited by severe testicular toxicity associated with oxidative stress, inflammation, apoptosis, and ferroptosis. Therefore, the present study investigated the protective effects of icariin-loaded nanoliposomal formulation (ICA-LNPs) against MTX-induced testicular injury in rats compared with crude icariin (ICA). Sixty adult male Sprague Dawley rats were randomly allocated into six groups: control, ICA, ICA-LNPs, MTX, MTX+ICA, and MTX+ICA-LNPs. MTX administration markedly impaired reproductive function, evidenced by significant reductions in testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), sperm count, motility, and viability, together with increased sperm abnormalities. MTX also disrupted the NRF2/HO-1/NQO1 signaling pathway, suppressed antioxidant defenses, and elevated oxidative stress markers. In addition, MTX significantly activated NF-κB-mediated inflammatory responses, enhanced apoptotic and ferroptotic pathways, increased iron accumulation and ACSL4 expression, and reduced GPX4 and SLC7A11 expression in testicular tissue. Histopathological examination further confirmed severe degeneration of seminiferous tubules and impaired spermatogenesis. Treatment with ICA-LNPs significantly ameliorated these alterations and demonstrated superior protective efficacy compared with crude ICA. ICA-LNPs restored reproductive hormones, improved semen quality, enhanced antioxidant status, suppressed inflammatory mediators, reduced apoptosis and ferroptosis-related markers, and preserved normal testicular histoarchitecture. Furthermore, GPX4 immunoreactivity was markedly increased, whereas ACSL4 expression was significantly reduced following ICA-LNPs treatment. In conclusion, ICA-loaded nanoliposomal formulation effectively attenuated MTX-induced testicular toxicity and was associated with reduced oxidative stress, inflammation, apoptosis, and ferroptosis, highlighting its potential as a promising therapeutic strategy for preserving male reproductive function. - Source: PubMed
Publication date: 2026/08/13
Alemam AhmedJamil SalimHassan HeshamElmorsy Ekramy M - This study evaluated dietary quercetin supplementation to investigate the effects of increasing inclusion levels on growth performance, diarrhea, serum health-related indicators, and whole-blood gene expression in weaned piglets. In a 28-day feeding trial, 128 piglets received diets formulated to contain 0, 100, 200, or 300 mg/kg quercetin (four pens of eight piglets per treatment; pen as the experimental unit). Final body weight and average daily gain were higher in the 200 and 300 mg/kg groups than in the control, and the 300 mg/kg group had the highest gain-to-feed ratio (G:F) ( < 0.05). Diarrhea rate declined linearly ( < 0.001); the rate in the 300 mg/kg group was lower than in the control and 100 mg/kg groups but did not differ from the 200 mg/kg group. Quercetin reduced serum malondialdehyde, pro-inflammatory cytokines, urea nitrogen, and aspartate aminotransferase, while increasing total protein, albumin, total antioxidant capacity, several antioxidant enzyme activities, and interleukin-10 ( < 0.05). Serum diamine oxidase activity and D-lactate concentration also declined linearly ( < 0.001). Whole-blood expression of decreased; , , and increased; and was unchanged. Overall, within the tested range, increasing dietary quercetin improved growth and feed efficiency, reduced diarrhea, and was accompanied by coordinated changes in serum health-related indicators and whole-blood transcripts. - Source: PubMed
Publication date: 2026/08/06
Li YizhuoShao LinsenGuan XuanchengXie LiyuanQiao DaChen JingLiu Xianjun - : This study aimed to identify common target genes, molecular interaction networks, and signaling pathways shared across the investigated toxic metal(loid)s-lead (Pb), cadmium (Cd), methylmercury compounds (MMC), arsenic (As), nickel (Ni), and hexavalent chromium (Cr(VI))-and associated with lung cancer overall, non-small-cell lung cancer (NSCLC), and small-cell lung cancer (SCLC). : The Comparative Toxicogenomics Database (CTD) was used to identify associated genes, GeneMANIA to characterize molecular interaction networks, and ToppFun for pathway enrichment analysis. : Two common genes ( and ) were identified for SCLC, eight for NSCLC (, , , , , , , and ), and eighteen for lung cancer overall. Gene network analysis revealed predominantly physical interactions in SCLC, pathway interactions in NSCLC, and co-expression in lung cancer overall. Several toxic metal(loid)s exhibited concordant effects on TP53, VEGFA, HMOX1, and IL6 expression. was the only gene common to all investigated toxic metal(loid)s and lung cancer categories. Pathway enrichment identified PI3K-AKT-mTOR signaling in both SCLC and NSCLC, VEGF signaling in NSCLC, and MAPK, interleukin, and macrophage-stimulating protein (MSP) signaling in lung cancer overall. : The identified genes and pathways suggest molecular mechanisms potentially relevant to the association between exposure to the investigated toxic metal(loid)s and lung carcinogenesis, particularly those related to cell survival, inflammation, oxidative stress, and angiogenesis. may represent a common molecular link warranting further investigation. The identified pathways represent candidate biomarkers and mechanistic targets, highlighting the biological heterogeneity of lung cancer and the importance of subtype-specific analyses. - Source: PubMed
Publication date: 2026/07/25
Živančević KatarinaKök Kıvanç - Chronic exposure to lead (Pb) represents a persistent environmental hazard that can impair hippocampal integrity and cognitive function, while effective protective strategies remain limited. Ginsenoside Rg1 is an important bioactive constituent derived from and has been reported to possess antioxidant and neuroprotective activities; however, its involvement in Pb-triggered ferroptosis-associated neuronal damage remains unclear. In the present study, a male C57BL/6J mouse model of subchronic lead acetate exposure and a lead-exposed HT22 cell model were established. Behavioral and histopathological changes were assessed, followed by analysis of inflammatory responses, oxidative stress, ferroptosis-related alterations, and Nrf2-associated signaling. Rg1 improved cognitive performance and attenuated hippocampal neuronal loss, neuroinflammatory activation, oxidative injury, and ferroptosis-related alterations, including ferrous ion accumulation and mitochondrial damage. Consistently, Rg1 restored SLC7A11/xCT and GPX4 expression and enhanced Nrf2-associated antioxidant signaling, whereas the Nrf2 inhibitor ML385 weakened the Rg1-induced increases in nuclear Nrf2, NQO1, and GPX4. Collectively, these findings indicate that Rg1 alleviates lead-induced neurotoxicity and support the involvement of Nrf2 signaling in the regulation of oxidative stress and ferroptosis-related injury. These findings provide experimental evidence supporting further preclinical investigation of Rg1 and its Nrf2-associated neuroprotective mechanisms in Pb-induced neuronal injury. - Source: PubMed
Publication date: 2026/07/23
Gong YiyaoZhang JieWang TingtingLi XiangWang HaoRen Li - Atherosclerosis progression is closely linked to metabolic dysfunction of plaque macrophages, where inducible nitric oxide synthase (iNOS)-mediated pathological nitric oxide (NO) burst is a key driver of inflammation and oxidative stress. This study designed macrophage membrane-camouflaged liposomes (M-AN@Lip) for the co-delivery of nicotinamide mononucleotide (NMN) and L-arginine (L-Arg), aiming to precisely regulate macrophage NO metabolic homeostasis. In vitro experiments demonstrated that M-AN@Lip effectively increased intracellular NO generation while significantly downregulating the expression of the oxidative stress-related enzyme NAD(P)H quinone oxidoreductase 1 (NQO1), suggesting a reprogramming of macrophage NO metabolism from a pathological iNOS-dominated pathway towards a protective one. This metabolic shift was accompanied by clearance of intracellular reactive oxygen species (ROS), enhancement of the endogenous antioxidant enzyme system, and polarization of macrophages towards an anti-inflammatory M2 phenotype. Ultimately, M-AN@Lip significantly inhibited oxidized low-density lipoprotein (ox-LDL) uptake and foam cell formation by downregulating the expression of scavenger receptors (CD36, MSR1, SRB1). This study demonstrates that a biomimetic nano-system can achieve integrated anti-inflammatory, antioxidant, and anti-foam cell forming effects through the synergistic regulation of NO metabolism, offering a promising novel nanotherapeutic strategy for atherosclerosis. - Source: PubMed
Publication date: 2026/08/12
Li XutingYuan YiLian ChanghongZhu DongdongWang YanJia Zhenlei