Human lipocalin 2,LCN2 ELISA Kit
- Known as:
- Human lipocalin 2,LCN2 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-1430
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human lipocalin 2 LCN2 ELISA Kit
Related genes to: Human lipocalin 2,LCN2 ELISA Kit
- Gene:
- LCN2 NIH gene
- Name:
- lipocalin 2
- Previous symbol:
- -
- Synonyms:
- NGAL, 24p3
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2016-10-05
Related products to: Human lipocalin 2,LCN2 ELISA Kit
Related articles to: Human lipocalin 2,LCN2 ELISA Kit
- This study aimed to investigate the regulatory effect of lipocalin-2 (LCN2) knockdown on DHODH-mediated mitochondrial ferroptosis in sepsis-induced myocardial injury (SIMI) and clarify the underlying STAT3-related molecular mechanism in a cecal ligation and puncture (CLP) mouse model and lipopolysaccharide (LPS)-stimulated HL-1 cardiomyocyte injury model. We established a classic cecal ligation and puncture (CLP)-induced SIMI mouse model. Pharmacological suppression of ferroptosis was performed to confirm the pathogenic role of ferroptosis in SIMI progression. Subsequently, LCN2-knockdown mice were utilized to explore the biological function of LCN2 in modulating myocardial ferroptosis and septic cardiac injury, and the direct protein interaction between LCN2 and DHODH was verified via molecular docking and co-immunoprecipitation assays. In vitro, we constructed stable DHODH-overexpressing HL-1 cardiomyocytes via lentiviral transfection and established a lipopolysaccharide (LPS)-induced cardiomyocyte injury model. The results showed that LCN2 expression was markedly upregulated in SIMI. Both GPX4- and DHODH-dependent mitochondrial ferroptosis were significantly activated during SIMI. Lentivirus-mediated DHODH overexpression exerted prominent protective effects against LPS-induced cardiomyocyte injury. Importantly, pharmacological blockade of DHODH by Brequinar reversed the reduction of p-STAT3 induced by LCN2 silencing. However, Fin56-mediated specific inhibition of mitochondrial GPX4 exhibited no significant effect on STAT3 phosphorylation level, revealing distinct regulatory mechanisms for these two pathways. In summary, LCN2 knockdown inhibits DHODH-mediated mitochondrial ferroptosis to alleviate SIMI. Pharmacological inhibition of DHODH abrogates the cardioprotective effect of LCN2 knockdown by restoring STAT3 phosphorylation. These findings provide novel insights into the prevention and treatment of sepsis-induced myocardial injury. - Source: PubMed
Publication date: 2026/08/03
Li LuLi YupingHao YixuanYu MengjieXia ShichengWang JiahuiYe HongweiGao Qin - This study investigated the impact of human immunodeficiency virus (HIV) infection and combination antiretroviral therapy (cART) on adipokine concentrations, which are bioactive molecules secreted by adipose tissue and involved in the regulation of metabolism and inflammation. Alterations in adipokine levels may contribute to the metabolic disturbances observed in people living with HIV. The analyzed adipokine panel included resistin, visfatin, chemerin, angiopoietin-like protein 2 (ANGPTL2), lipocalin-2 (LCN2), Wnt family member 5A (Wnt5a), adiponectin, omentin, vaspin, secreted frizzled-related protein 5 (SFRP5), and apelin. Blood samples were collected from people living with HIV and HIV-negative control participants. Adipokine concentrations were measured using an enzyme-linked immunosorbent assay (ELISA). Patients were further stratified according to their cART regimen, including either protease inhibitor (PI)-based or integrase strand transfer inhibitor (INSTI)-based therapy. Plasma concentrations of ANGPTL2 and vaspin were significantly higher, whereas concentrations of visfatin, SFRP5, and adiponectin were significantly lower in HIV-infected patients compared with controls. Comparison of patients receiving INSTI- or PI-based regimens with the control group revealed significant differences in visfatin, SFRP5, and adiponectin concentrations. Notably, adiponectin concentrations were significantly lower in the INSTI-treated subgroup than in patients receiving PI-based therapy. These findings suggest that five of the examined adipokines may be associated with HIV infection and cART exposure, potentially contributing to the development of metabolic disturbances in this population. Further studies involving larger cohorts of individuals with HIV receiving long-term cART are required to better elucidate the relationship between adipokine alterations and the risk of treatment-related metabolic complications. - Source: PubMed
Publication date: 2026/08/01
Szymańska BeataKnysz BrygidaPiwowar Agnieszka - Short-term heat acclimation (HA) induces cardiovascular and fluid-regulatory adaptations, but it's impact on markers of renal tubular injury and acute kidney injury risk (AKI) during exercise-heat stress remains unclear. Fourteen healthy endurance-trained male athletes were randomised to five days of isothermic HA (HOT; n = 7; 32 °C, 70% relative humidity; target core temperature ≥38.5 °C), or exercise in thermoneutral conditions (TEMP, n = 7). Heat stress tests (HST; 45 min cycling at 32 °C, 70% RH) were performed pre- and post-intervention. Blood biomarkers of kidney tubular stress (NGAL, KIM-1), fluid-regulation (copeptin, serum osmolality) and sympathetic activity (plasma normetanephrine) were measured at rest and immediately post-HST. HA reduced resting heart rate (-8 ± 5 bpm, p = 0.007, d = 1.0), increased plasma volume (+7.3 ± 5.1%, p = 0.022) and sweat loss (+500 ± 539 mL, p = 0.018, d = 1.1). Copeptin rose during the pre-intervention HST in both groups (HOT: + 11 ± 6; TEMP: + 12 ± 13 pmol·L ⁻ ¹, p < 0.05), but not post-intervention. NGAL increased only in TEMP during HST1 (+45 ± 29 μg·L ⁻ ¹, p = 0.030), while KIM-1 remained unchanged. No group x time interactions were observed for any biomarkers (p > 0.05). Five days of HA improved cardiovascular and thermoregulatory responses but did not alter renal stress markers or fluid-regulatory responses during exercise in the heat. These findings suggest short-term HA enhances heat tolerance but may not attenuate renal biomarker responses associated with early tubular stress under hot, humid conditions. - Source: PubMed
Publication date: 2026/08/11
Snape DanielWainwright BarneyParsons Iain TStacey Michael JWoods David RO'Hara John - Traumatic optic nerve and retinal injuries can lead to severe visual impairment, with undetermined underlying molecular mechanism and few reliable molecular biomarkers. This study aims to identify dysregulated genes and signaling pathways potentially involved in these injuries. - Source: PubMed
Publication date: 2026/07/27
Li JinjunZhang YongZhou Shu - To investigate the protective effect of lipocalin-2 (LCN2) gene knockout against sepsis-induced acute lung injury (ALI) and vascular endothelial dysfunction in mice and the mediating role of the nuclear factor-κB (NF-κB) signaling pathway. - Source: PubMed
Yu MengjieZhao AnboHao YixuanWang YirenLiu YuexianYe HongweiGao Qin