Ask about this productRelated genes to: CYP2E1 antibody
- Gene:
- CYP2E1 NIH gene
- Name:
- cytochrome P450 family 2 subfamily E member 1
- Previous symbol:
- CYP2E
- Synonyms:
- -
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-03-03
- Date modifiied:
- 2015-12-09
Related products to: CYP2E1 antibody
Related articles to: CYP2E1 antibody
- Immune checkpoint inhibitors elicit responses in merely 20-40% of patients with microsatellite instability-high or mismatch repair-deficient colorectal cancer (CRC), making immunotherapy resistance a formidable clinical challenge. The immunosuppressive tumor microenvironment, characterized by regulatory T-cell accumulation and metabolic reprogramming, substantially drives this treatment failure. - Source: PubMed
Publication date: 2026/04/23
Zhang XiaochunYang YangZhang MeiqiXu YanyanWang JunZhang ChunxiaGu JiaboLiu JianleiYe XiaoruiZhang XinyiJin Heiying - Tuberculosis (TB) remains a major public health challenge in Peru, where interindividual variability in treatment response and drug-induced hepatotoxicity may be influenced by host genetic background. This study aimed to characterize clinically relevant polymorphisms in , , and in a cohort of TB patients from Southern Peru, a genetically underrepresented Andean population. Thirty-five adults receiving first-line therapy (isoniazid and rifampicin) underwent targeted Sanger sequencing of key functional variants among these three genes. acetylator phenotypes were predominantly intermediate (68.6%), followed by rapid (20%) and slow (11.4%) profiles, with high minor allele frequencies for rs1041983 and rs1801280. functional promoter variants were infrequent, whereas exhibited notable allelic heterogeneity, suggesting potential variability in rifampicin transport. Comparative analysis with previously reported Peruvian data revealed regional differences in acetylator distribution, supporting population-specific pharmacogenomic stratification. Although clinical toxicity outcomes were not evaluated, the high prevalence of reduced acetylation genotypes suggests a substantial proportion of patients may benefit from genotype-informed isoniazid dosing strategies. These findings provide foundational data for implementing precision medicine approaches using affordable and targeted technologies in TB management within Andean populations and support the integration of pharmacogenomics into national TB control programs. - Source: PubMed
Publication date: 2026/03/29
Chavez-Arias TatianaManrique-Sam CeciliaIta-Balta YumaMontánchez-Carazas EdgarMurillo Carrasco Alexis GermánFarfán-Delgado Miguel - Acute lung injury (ALI) induced by lipopolysaccharide (LPS) is characterized by pulmonary edema, inflammatory cell infiltration, and alveolar epithelial damage. Here, we investigated the protective effects of 4-Methyl-5-Acetylthiazole (Q11), a novel CYP2E1 inhibitor, against LPS-induced ALI. Q11 significantly reduced lung index, wet-to-dry ratio, histopathological injury, and bronchoalveolar lavage fluid protein and cell content in LPS-induced ALI mice, indicating a protective effect of Q11 against ALI. Mechanistically, Q11 suppressed CYP2E1 level and inhibited M1 macrophage polarization, reducing pro-inflammatory cytokines in lung tissue, bronchoalveolar lavage fluid, and serum. Additionally, Q11 mitigated oxidative stress, restored mitochondrial membrane potential and ATP production, balanced mitochondrial dynamics, and attenuated apoptosis in alveolar epithelial cells and macrophages. In vitro, Q11 did not directly protect epithelial cells from LPS-induced injury but indirectly improved epithelial viability and reduced apoptosis via modulation of macrophages in a conditioned medium co-culture system. Collectively, these findings demonstrate that Q11 protects against LPS-induced ALI by inhibiting CYP2E1-mediated M1 macrophage activation, alleviating oxidative stress, preserving mitochondrial function, and indirectly safeguarding epithelial cells. Our results suggest that Q11, as a novel CYP2E1 inhibitor, exhibits promising translational potential and represents a potential therapeutic strategy for ALI. - Source: PubMed
Publication date: 2026/04/24
Gao LiyuanWang MengyuYang RuiQiu JinhuanJia LinDeng MengyanTang LimingWen QiangXu HaiweiGao NaQiao Hailing - Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease globally, yet effective therapeutic options remain limited. Red-fleshed apples are rich in dietary flavonoids, but their chemical basis and therapeutic potential for MASLD have not been systematically explored. This study integrated LC-MS/MS metabolomics with a high-fat diet (HFD)-induced MASLD mouse model to evaluate the therapeutic effects and mechanisms of 'XJ4' red-fleshed apple flavonoid extracts (RAFEs). Metabolomics identified 120 types of flavonoids in white-fleshed apple 'FJ' and red-fleshed apple 'XJ4', and 57 differentially accumulated metabolites have been detected in both, among which 39 flavonoids significantly accumulated higher in 'XJ4'. Compared with 'FJ', 'XJ4' was predominantly enriched in -glycosylated flavonols, including isorhamnetin 3--glucoside, cacticin, tamarixin, reynoutrin, and guaijaverin. Male ICR mice were randomly divided into nine groups ( = 10): three groups, normal control, HFD model control, and positive control, receiving simvastatin, 10 mg kg, and six groups receiving RAFEs or white-fleshed apple flavonoid extracts (WAFEs) at low, medium, or high doses (1, 3 and 5 mg kg). Hepatic parameters were assessed by histopathological analysis, biochemical assays, RT-qPCR, immunofluorescence, and western blot analysis; the gut microbiota composition was analysed by 16S rRNA gene sequencing. Medium-dose RAFEs (3 mg kg) conferred optimal efficacy, significantly reducing body weight gain, liver coefficient, and plasma ALT, AST, and ALP levels while restoring the hepatic histological architecture. Mechanistically, RAFEs suppressed pro-inflammatory mediators (IL-6, IL-1β, NF-κB, IRF6 and TLR4) and the oxidative stress marker CYP2E1, while enhancing antioxidant capacity (SOD, CAT and T-AOC). RAFEs also reduced hepatic TG, TC, and LDL-C, increased HDL-C, and modulated lipid metabolism AMPK and PPAR-α upregulation with α-SMA suppression. Furthermore, RAFEs restored gut microbiota diversity, enriched beneficial taxa (, and ), and suppressed pathogenic . RAFEs consistently outperformed WAFEs, attributable to XJ4's unique isorhamnetin-dominated flavonol glycoside profile. These findings support red-fleshed apple flavonoids as promising natural agents for MASLD treatment. - Source: PubMed
Publication date: 2026/04/20
Chen YizhouDong YaqiFan ZhaozhengJiang ShenghuiWu YaWang ChengkunZhu TongyaoWang ZhongkangGuo ShaoxiaZhang YugangLiang Xiao - This study investigated the hepatoprotective effects of a combined ethanolic extract of Moringa oleifera and methanolic extract of Urtica dioica (MU), F3 (2:1 w/w), against isoniazid (INH) and rifampicin (RIF)-induced liver toxicity in rats. Formulation F3, characterized by high total phenolic (246.45 ± 1.80 µg GAE/mg) and flavonoid (67.07 ± 0.21 µg QE/mg) contents, exhibited potent in vitro antioxidant activity (e.g., DPPH IC50 of 42.66 ± 0.59 µg/mL for F3). Significantly, oral administration of F3 alone (200, 400 mg/kg) did not induce liver toxicity, maintaining normal histopathology similar to controls. Conversely, INH-RIF treatment significantly increased serum liver markers (AST, ALT, ALP, bilirubin, and triglycerides), elevated MDA levels, reduced CAT and GSH activities, and caused severe histopathological damage. The combined extract F3, particularly at 400 mg/kg, significantly reversed these biochemical and histopathological alterations. In silico ADMET, DFT, and docking analyses elucidated multi-targeted mechanisms: DFT predicted high reactivity for compounds such as riboflavin (5a), correlating with antioxidant effects. Docking showed strong binding of oleuropein (3a) and riboflavin (5a) to CYP2E1 and TNF-α, suggesting inhibition of toxic metabolite formation and inflammation. These findings highlight this natural combination's potential as an adjunctive therapy for anti-tuberculosis drug-induced liver injury. - Source: PubMed
Boutaoui NassimaLariche NesrineStiti Mohamed ZakariaSaidi Katia MohandBousbaa WalidRebbas KhellafHarrouche KamelKhelili Smail