Nrf2 Polyclonal pAb
- Known as:
- Nrf2 Polyclonal pAb
- Catalog number:
- ASAKAP-TF125D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Nrf2 Polyclonal pAb
Related genes to: Nrf2 Polyclonal pAb
- Gene:
- KEAP1 NIH gene
- Name:
- kelch like ECH associated protein 1
- Previous symbol:
- -
- Synonyms:
- KIAA0132, MGC10630, MGC1114, MGC20887, MGC4407, MGC9454, INrf2, KLHL19
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-30
- Date modifiied:
- 2015-11-23
Related products to: Nrf2 Polyclonal pAb
Related articles to: Nrf2 Polyclonal pAb
- Contrast-associated acute kidney injury (CA-AKI) is a clinically relevant complication of iodinated contrast exposure. This study investigated whether gallic acid (GA) attenuates diatrizoate (Urografin 76%; URO)-induced renal injury in rats and whether this effect is associated with nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1 (Keap-1)/heme oxygenase-1 (HO-1) transcript-level changes. - Source: PubMed
Publication date: 2026/08/21
Akyürek Bayhan NurhanGündüz DemetFatih Karakuyu NasıfIlhan İlterYusuf Tepebaşi MuhammetBerk Imeci OrhanSarman EmineSavran Mehtap - In this work, two previously undescribed sesquiterpenes, beilschmiedins A-B (1-2), as well as twelve known compounds (3-14), were obtained from the methanol extract of the () leaves. Their structures were fully elucidated using a combination of spectroscopic techniques, including HR-ESI-MS, UV, and 1D/2D NMR, and compared with literature data. Furthermore, the absolute configurations of the new compounds 1 and 2 were determined by quantum chemical ECD calculations. Biologically, the fourteen isolates were evaluated for their anti-inflammatory, enzyme inhibitory, and antioxidant activities. Eleven compounds inhibited NO production more strongly than the positive control l-NAME. Among them, phillygenin (4), -pinoresinol (5), fargesin (6), and schisandlignan A (11) showed the most potent inhibitory effects (IC = 9.8-17.2 µM). In enzyme inhibition assays, schisandlignan A (11) and 3',4'-dimethoxybenzoic acid (3″,4″-dimethoxyphenyl)-2-methyl-3-oxobutyl ester (14) exhibited exceptional α-glucosidase inhibitory potential (IC = 6.2 ± 0.38 and 5.0 ± 0.46 µM, respectively), significantly outperforming acarbose, while kobusin (7), forsythialan B (8), and nectandrin E (13) showed moderate xanthine oxidase inhibition (IC = 74.7-127.6 µM). For antioxidant activity, compound 5 possessed the strongest radical scavenging capacity, revealing that free phenolic hydroxyl groups enhanced potency. Furthermore, this study provides the first report of the anti-inflammatory activity of 11 and the α-glucosidase inhibition of 11 and 14, whereas the two new sesquiterpenes, 1 and 2, displayed only moderate anti-inflammatory effects and were inactive in the other assays. Molecular docking studies demonstrated that these bioactive compounds exhibit favorable binding affinities toward COX-2, XO, α-glucosidase, and Keap1, supporting their potential anti-inflammatory, antioxidant, antidiabetic, and anti-gout activities. The 200 ns molecular dynamics simulations further revealed stable complex behavior and limited structural deviation of the selected ligands within their respective binding sites. - Source: PubMed
Publication date: 2026/08/20
Tran-Trung HieuXuan Duc DauChung Nguyen ThiHung Phan QuocVan Trung HoangVan Quoc NguyenNguyen-Ngoc HieuVan Anh CaoPham Duc-VinhHa Nguyen XuanGiang Le Duc - Diabetic nephropathy (DN) is a major complication that arises from diabetes. Curcumin, a bioactive compound with antioxidant properties, has been shown to modulate multiple cellular pathways and thereby mitigate tissue damage. - Source: PubMed
Li YuWang Lu-LuYu Xiang-ZhiXie SaiLi Peng-FeiHuang YangBao Pei-Ling - Ischemic stroke is an unmet therapeutic need, characterised by excessive oxidative stress, mitochondrial impairment, blood-brain barrier (BBB) damage, and neuronal cell death. 4-Octyl itaconate (4-OI) is known for its promising antioxidant properties; however, its effects in cerebral ischemia/reperfusion (I/R) injury have not been previously explored. In this study, middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R) models were used to mimic the cerebral I/R injury. Treatment with 4-OI significantly improved neuronal survival and neurological outcomes, reduced oxidative damage and mitochondrial dysfunction. Mechanistically, 4-OI markedly attenuated intracellular and mitochondrial ROS, restored mitochondrial membrane potential, and inhibited neuronal apoptosis. Furthermore, 4-OI treatment exerts its neuroprotective effect by suppressing lipid peroxidation and modulating the Nrf2/HO-1/SLC7A11/GPX4 axis to inhibit ferroptosis and BBB damage. Pharmacological inhibition of Nrf2 using ML-385 abolished the effects of 4-OI, confirming the essential role of Nrf2 activation in mediating ferroptosis suppression. Additionally, molecular docking analysis revealed favourable binding of 4-OI to Keap-1, supporting a potential mechanism by which 4-OI impede the Keap1-Nrf2 interaction to promote Nrf2 activation. Collectively, these findings suggest that 4-OI confers Neuroprotection against I/R injury by activating Nrf2 pathway, reducing oxidative stress, and suppressing ferroptotic and apoptotic cell death. This study identifies 4-OI as a promising therapeutic candidate for cerebral I/R injury and highlights the Nrf2-mediated ferroptosis pathway as a potential target for neuroprotection. - Source: PubMed
Publication date: 2026/08/20
Chauhan ChandanKaundal Ravinder K - Ferroptosis is a critical contributor to chemotherapy-induced liver injury. Schisandrin B (SchB), a bioactive compound from Schisandra chinensis, exerts hepatoprotection, but the underlying mechanisms in oxaliplatin (OXA)-induced liver injury are unclear. In this study, OXA treatment induced hepatic dysfunction, lipid accumulation, and gut dysbiosis, with marked depletion of Lactobacillus reuteri (L. reuteri). A lipidomic analysis showed that SchB reversed OXA-induced linoleic acid (LA) metabolic reprogramming, particularly PE (18:0_18:2) and PE (18:2_18:2) accumulation. A targeted quantification revealed that OXA increased the levels of the LA-derived oxidation products 9-HODE and 13-HODE, which were significantly reduced by SchB treatment. Mechanistically, SchB mitigated OXA-induced DILI by suppressing ferroptosis through the dual-targeted activation of Nrf2. Notably, in addition to the canonical KEAP1-dependent mechanism, an important gut microbiota-mediated pathway appeared to contribute substantially to Nrf2 activation. SchB reshaped the gut microbiota by enriching L. reuteri, which metabolized the accumulated LA into conjugated linoleic acid (CLA). The CLA contributed to Nrf2 activation via a microbiome-dependent non-canonical pathway. Nrf2 knockout rats and FMT experiments further confirmed the causal roles of Nrf2 and L. reuteri in SchB-mediated hepatoprotection against lipid peroxidation. Importantly, in microbiota-depleted rats with OXA-induced liver injury, CLA supplementation partially restored Nrf2 activation and attenuated lipid peroxidation, indicating that CLA positively affected the microbiota-dependent hepatoprotective pathway associated with SchB. Collectively, these findings identify SchB as a potent therapeutic candidate against OXA-induced liver injury and highlight a microbiota-driven L. reuteri-CLA-Nrf2 axis as a key non-canonical pathway regulating gut-liver metabolic crosstalk and ferroptosis to maintain hepatic homeostasis. - Source: PubMed
Publication date: 2026/08/20
Huang PingLi ShanLiu YichenLi JinyingLiu BingchenLi NaWang ChengXia ChunhuaLiu Fanglan