Ask about this productRelated genes to: HEBP1 antibody
- Gene:
- HEBP1 NIH gene
- Name:
- heme binding protein 1
- Previous symbol:
- -
- Synonyms:
- HEBP, HBP
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-16
- Date modifiied:
- 2016-10-05
Related products to: HEBP1 antibody
Related articles to: HEBP1 antibody
- There is growing evidence supporting the anti-inflammatory activity of plant sterols (PS) in preclinical models of intestinal inflammation. However, the underlying mechanisms driving these beneficial effects remain incompletely understood. This study investigates the transcriptional modulatory activity of a PS food supplement (PS-FS) on genes associated with the cellular antioxidant defense system and tight junction (TJ) proteins. A double-chamber coculture model with differentiated Caco-2 cells (apical) and RAW264.7 macrophages (basolateral) was used. Bioaccessible fraction (BF) of PS-FS was obtained following the INFOGEST 2.0 simulated gastrointestinal digestion. A 1/20 dilution of BF was applied to the apical chamber for 90 min, followed by lipopolysaccharide (LPS) stimulation (1 µg/mL, 24 h) on the basolateral side. The interaction between PS-FS and budesonide was also evaluated. The gene expression of Nrf2 (NFE2L2), glutathione S-transferase A1 (GSTA1), NAD(P)H quinone dehydrogenase 1 (NQO1), and heme oxygenase 1 (HMOX-1) was quantified. Additionally, gene expression of TJ-related genes (CLDN1, CLDN3, CLDN4, OCLN, and TJP1) was quantified. Pretreatment with PS-FS significantly increased expression of GSTA1 (26.8%) and HMOX-1 (124.4%) compared to LPS + digestion blank. Furthermore, there was a trend toward increased expression of NFE2L2 and NQO1. Similarly, PS-FS enhanced expression of CLDN3 (33.0%), CLDN4 (211.7%), OCLN (57.1%), and TJP1 (98.9%). However, co-treatment of budesonide and PS-FS resulted in antagonistic interactions. These findings indicate that PS-FS modulates gene expression associated with antioxidant responses and intestinal barrier integrity-related pathways, suggesting to be further developed as a dietary strategy to support the management of inflammatory bowel disease PRACTICAL APPLICATIONS: This research supports the potential use of plant sterol-based food supplements in products aimed at supporting intestinal health. The results suggest that these supplements could help strengthen the gut barrier and support the body's natural antioxidant defenses during intestinal inflammation. - Source: PubMed
Makran MussaGiardina Ilenia ConcettaGarcia-Llatas GuadalupeAttanzio AlessandroCilla Antonio - This study systematically characterizes ferroptosis-mediated antitumor mechanisms of exosome-like nanovesicles derived from Scutellaria barbata D. Don (SBENs) in hepatocellular carcinoma (HCC). SBENs were isolated by ultracentrifugation combined with sucrose gradient centrifugation and characterized by NTA, TEM, and DIA-based proteomic analysis. Ferroptosis induction was assessed in HepG2 cells and subcutaneous xenograft models through biochemical assays, qPCR, Western blot, and histopathological examination. SBENs were isolated using ultracentrifugation and sucrose gradient centrifugation. NTA and TEM revealed subspherical SBENs with an average diameter of 134.1 nm. Proteomic analysis identified modulation of ferroptosis-related proteins. Cellular assays showed SBENs suppressed HepG2 proliferation, migration, invasion, and ferroptosis. The ferroptosis effect induced by SBENs in HepG2 cells is marked by mitochondrial depolarization, elevated Fe²⁺, MDA, ROS, depleted GSH, and reduced SLC7A11/GPX4 expression. Mitochondrial dysfunction involved downregulated ND1, CYTB, COX1 and TFAM suppression, mechanistically associated with Nrf2/SLC7A11/GPX4 pathway inhibition. In xenografts, SBENs attenuated tumor growth, reduced Ki-67 expression, and induced ferroptosis without altering serum ALT, AST, BUN, CRE levels or causing histological damage. SBENs induced HepG2 ferroptosis via mitochondrial dysfunction and Nrf2/SLC7A11/GPX4 pathway inhibition, effectively triggering HCC ferroptosis in subcutaneous tumor xenografts with safety profiles. - Source: PubMed
Publication date: 2026/05/29
Liang ZichengFang XiayiTao MengjuanZhang ZhenTan XiaoningZeng Puhua - To explore the mechanism mediating the ameliorative effect of Granules on cartilage injury in knee osteoarthritis (KOA). - Source: PubMed
Cheng YuanyuanHuang ChuanbingZhang JuanZhu YawenQian Ai - In the context of the circular economy, the valorization of natural biomolecules from by-products has recently represented a major goal in health promotion. From this perspective, this study examined the antioxidant potential of Sicilian white grape pomace from the Pinot Gris variety, using subcritical water extraction as an eco-friendly and innovative method to recover bioactive compounds. Different extraction parameters allowed for comparing the potential of various fractions. Among these, the Subcritical Water Extract obtained after 5 min at 160 °C (SWE) was rich in gallic acid and protocatechuic acid, as evidenced by characterization with UHPLC-Q Exactive Orbitrap-HRMS system. SWE showed efficacious antioxidant activity, as confirmed by DPPH assay and total polyphenol and flavonoid content. Interestingly, SWE displayed cytotoxic activity in tumor cell lines, while preserving the viability of non-tumor bronchial epithelial cells. Specifically, SWE protected these cells from exogenous oxidative stress, reducing the ROS levels and activating Nrf2-mediated antioxidant response. Surprisingly, upregulation of antioxidant enzymes (HO-1 and SOD-2) induced by SWE was maintained in the presence of lipopolysaccharide, indicating a specific involvement of SWE in the anti-inflammatory response. Finally, SWE was also able to limit the formation of stress granules following acute stress, thereby supporting its potential to maintain cellular homeostasis. Overall, this study highlights the potential of grape pomace as a source of active molecules to prevent oxidative stress and inflammation. - Source: PubMed
Publication date: 2026/05/19
Affranchi FedericaPratelli GiovanniRaimondo RaffaeleKiselev PavelGiuliano MichelaNotaro AntoniettaEmanuele Sonia - Accumulating evidence suggests that vitamin B6 (B6) deficiency among older adults is associated with sarcopenia, frailty, heart disease, and brain diseases. Oxidative stress and inflammation play key roles in cardiac and skeletal muscle and neuronal pathology. However, the detailed roles of B6 supplementation in oxidative stress and inflammation are not fully understood. Recent studies have shown that supplemental B6 upregulated the nuclear factor erythroid 2-like 2 (Nrf2) signaling pathway with the coordinated activation of antioxidant responses. Accumulating evidence suggests the potential of targeted Nrf2 signaling regulation in the treatment of aging-related musculoskeletal, heart, and brain diseases. Notably, dietary supplementation of B6 elevates the levels of several antioxidant metabolites, such as carnosine, anserine, taurine, hydrogen sulfide (HS), 5-methyltetrahydrofolate, kynurenic acid, 3-hydroxyanthranilic acid, and γ-aminobutyric acid (GABA) via the upregulation of pyridoxal 5'-phosphate (PLP)-dependent metabolic pathways, thereby linking to Nrf2 signaling activation. Furthermore, supplemental B6 stimulates glycogen breakdown through the PLP enzyme, glycogen phosphorylase, which in turn enhances the pentose phosphate pathway, thereby increasing nicotinamide adenine dinucleotide phosphate (NADPH) availability to regenerate glutathione (GSH). In this perspective article, we propose the potential role of B6 as an antioxidant mediated by the PLP-dependent multi-metabolic productions of antioxidant metabolites. - Source: PubMed
Publication date: 2026/05/08
Kato NorihisaYang YongshouKhedara AbdelkrimKumrungsee Thanutchaporn