CYP2E1 Antibody
- Known as:
- CYP2E1 Antibody
- Catalog number:
- csb-pa006425ea01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- CYP2E1 Antibody
Related 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
- : Paracetamol is widely used for acute pain management in orthopedic trauma; however, interindividual variability in analgesic response remains insufficiently understood. Cytochrome P450 2E1 (CYP2E1), a key enzyme involved in paracetamol metabolism and the formation of the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI), may contribute to this variability. This study aimed to investigate the relationship between CYP2E1 gene polymorphisms and the analgesic efficacy of paracetamol in patients with lower extremity fractures. : A total of 127 patients with lower extremity fractures and 100 healthy controls were included. All patients received 1000 mg of intravenous paracetamol. Pain intensity was assessed using the Visual Analog Scale (VAS) at baseline and at 30, 60, and 120 min after administration. Genotyping of CYP2E1 polymorphisms (*1A, *5B, *6, and *7B) was performed using PCR-RFLP. Differences in the VAS scores and analgesic response were analyzed according to genotype. : Paracetamol administration resulted in a significant reduction in pain scores at all time points ( < 0.001). Patients carrying the CYP2E15B variant exhibited significantly higher VAS scores and a weaker early analgesic response compared to non-carriers ( ≤ 0.001). Similarly, CYP2E11A carriers demonstrated higher pain scores across all time points ( < 0.05), although the magnitude of effect was less pronounced. No significant differences were observed for the CYP2E16 variant. Due to low frequency, CYP2E17B could not be reliably analyzed. : Paracetamol is an effective analgesic in patients with lower extremity fractures; however, CYP2E1 polymorphisms may modulate individual pain perception and early analgesic response. In particular, the *5B and, to a lesser extent, *1A variants are associated with higher pain scores. These findings support the potential role of pharmacogenetic approaches in personalized pain management. - Source: PubMed
Publication date: 2026/05/25
Kocabay BarışÖk NusretKocabay Sinem YenilÖk Zeynep DündarYörükoğlu Ali ÇağdaşLengerova GerganaBozhkova MartinaPetrov SteliyanKöseler Aylin - Excessive alcohol consumption induces hepatic injury primarily through cytochrome P450 2E1 (CYP2E1)-mediated reactive oxygen species (ROS) generation and disruption of redox homeostasis. This study investigated the hepatoprotective effects of the ethyl acetate fraction from leaves (DMLEAF) against ethanol-induced oxidative damage in vitro and in vivo. The protective mechanisms of DMLEAF were evaluated in HepG2 cells exposed to ethanol (400 mM, 24 h) and in an acute ethanol-induced liver injury mouse model. Cellular ROS levels, apoptosis, antioxidant enzyme activities, and nuclear factor erythroid 2-related factor 2 (Nrf2) translocation were assessed in vitro. Serum biochemical markers, histopathological changes, and hepatic CYP2E1 mRNA expression were analyzed in vivo. In HepG2 cells, DMLEAF significantly reduced intracellular ROS levels and apoptosis, improving cell viability by up to 27.2% and reducing apoptosis by approximately 32%. DMLEAF also attenuated the ethanol-induced decrease in antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) and promoted nuclear translocation of Nrf2. In mice, oral administration of DMLEAF significantly reduced serum alanine aminotransferase and aspartate aminotransferase levels, improved histopathological alterations, and suppressed hepatic CYP2E1 mRNA expression by 2.6-fold compared with ethanol-treated controls, while preventing the reduction in hepatic antioxidant enzyme activities. These findings suggest that DMLEAF mitigates alcohol-induced liver injury through suppression of CYP2E1-associated ROS production and activation of Nrf2-mediated antioxidant defense mechanisms. - Source: PubMed
Publication date: 2026/06/12
Eom TaeKilKim Ju-Sung - Environmental exposure to persistent and non-persistent endocrine-disrupting chemicals (EDCs), including per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), polycyclic aromatic hydrocarbons (PAHs), dioxins, phthalates, and bisphenols, has been increasingly associated with elevated cardiovascular disease (CVD) risk. Emerging evidence suggests the importance of gene-environment interactions in modulating individual susceptibility to EDC-related cardiovascular effects. This review summarizes current knowledge by synthesizing the main classes of EDCs, evaluating the evidence linking them to cardiovascular outcomes, and highlighting how genetic variability may modulate EDC-induced cardiovascular risk. Across the studies analyzed, the most extensively investigated genetic polymorphisms involve pathways related to oxidative stress regulation, xenobiotic metabolism and detoxification, hormone signaling, and lipid homeostasis. Variants in antioxidant defense genes, such as , , and , have been associated with increased hypertension risk and vascular dysfunction following exposure to bisphenols and PAHs. Polymorphisms in , , CYP1A2, CYP2E1, , and may influence susceptibility to cardiometabolic alterations and congenital heart defects, whereas variants in , , , and have been linked to obesity, dyslipidemia, and hypertension associated with PFAS, PBDEs, and bisphenols. A deeper understanding of gene-environment interactions is essential to advance preventive cardiology and mitigate the cardiovascular impact of environmental pollutants. - Source: PubMed
Publication date: 2026/06/21
Palazzo MariangelaGorini FrancescaSimonini LudovicaMinichilli FabrizioBorghini Andrea - Carnosine is widely recognized for its antioxidant and cytoprotective properties and is being increasingly used in dietary supplements. However, its effects in drug-induced liver injury remain insufficiently studied. This study aimed to investigate and compare the hepatoprotective and antioxidative effects of pure carnosine and an antioxidant-enriched commercial carnosine supplement in a murine model of paracetamol-induced hepatotoxicity. Adult male Swiss Webster mice were pretreated orally for seven days with carnosine or a commercial carnosine supplement prior to a single hepatotoxic dose of paracetamol. The serum biochemical parameters, hepatic oxidative stress markers, histopathology, and immunohistochemical expression of CYP2E1, COX-2, and Iba1 were evaluated 24 h after paracetamol administration. Paracetamol increased serum aminotransferases, lipid peroxidation, CYP2E1 expression, and histological liver injury. Pure carnosine pretreatment tended to exacerbate biochemical liver injury, whereas the commercial supplement attenuated lipid peroxidation, preserved bilirubin levels, and reduced histological damage. Both formulations decreased CYP2E1 expression and were associated with less necrosis and COX-2 immunoreactivity compared with paracetamol alone. Antioxidant enzyme activities and macrophage markers showed no consistent intergroup differences. These findings indicate that carnosine may not consistently exert hepatoprotective effects in acute drug-induced liver injury and that accompanying antioxidants may critically modify its biological actions. - Source: PubMed
Publication date: 2026/06/01
Zaklan DraganaMartić NikolaAndrejić Višnjić BojanaBosanac MilanaHadžistević SnežanaRašković AleksandarPavlović Nebojša - The mouse gene Lilrb4a, an ortholog of human leukocyte immunoglobulin-like receptor B4 (LILRB4), is markedly upregulated in microglia in Alzheimer's disease models and has been implicated in Apolipoprotein E (APOE)-related signaling. However, its contribution to amyloid pathology under an APOE4 background remains unclear. Here, 5xFAD mice carrying human APOE4 were used to assess the impact of Lilrb4a reduction by genetic deletion or antisense oligonucleotide treatment. Both approaches significantly reduced cortical amyloid plaque burden and APOE4-associated cerebral amyloid angiopathy without altering amyloid-β (Aβ) production. Bulk RNA sequencing identified enrichment of peroxisome proliferator-activated receptor (PPAR)-related and broader metabolic pathways in Lilrb4a-deficient mice. Consistently, biochemical analyses showed reduced p-SHP-2, NF-κB-p65, and p-STAT1, increased p-STAT3, and induction of anti-inflammatory and clearance-associated effectors, including Arg-1, TGF-β, and Cyp2e1. In primary microglia, pharmacological interrogation supported a functional contribution of PPAR-γ signaling to the enhanced Aβ uptake and degradation associated with Lilrb4a suppression, whereas PPAR-γ agonism recapitulated key pro-clearance phenotypes in vitro and attenuated amyloid pathology in vivo. Together, these data support Lilrb4a as an APOE4-associated microglial checkpoint candidate linked to impaired amyloid clearance and identify a PPAR-linked pro-clearance program as a potential downstream component of this response. - Source: PubMed
Publication date: 2026/06/22
Nie ChangxuYang RuixiWang XiaotongJia PingZhang XueqiDai YaqiBai XueDuan SijiaLi YufengZheng PengTian XinJiang LiWang Chao