lcn2  (Sino Biological)

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: RNA transcriptome sequence results of EAU and ART-treated groups. (A) KEGG pathway enrichment analysis for the identified differentially expressed genes (DEGs). (B) The profile of DEGs across experimental conditions. (C) Volcano plot visualizing the DEGs, with labels highlighting the top 10 upregulated and downregulated genes. (D) Gene Ontology (GO) functional enrichment analysis of DEGs. (E, F) Relative LCN2 protein expression levels across the CON, EAU, and ART groups. (G, H) Sensorgrams for the interaction of LCN2 and Artesunate. (I, J) Sensorgrams for the interaction of STAT3 and Artesunate. n = 3. ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Sequencing, Functional Assay, Expressing

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Clinical and Histopathological scores and expression of inflammatory cytokines among the Control (CON), EAU, ART-treated, and LCN2-inhibitor groups. (A, C) Clinical scores of the anterior segment. (B, D) Histopathological scores based on H&E-stained retinal sections (40× magnification). White arrows: inflammatory cell infiltration; Red arrows: destruction of retinal structure. (E, F) Quantification of LCN2 protein expression across groups. (G-J) Western blot analysis of IL-1β, IL-6, and TNF-α protein levels. (K-M) Cytokine concentrations (IL-1β, IL-6, TNF-α) were determined by ELISA. n = 3-6.** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Expressing, Control, Staining, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Expression of ferroptosis-related proteins, ROS, and SOD in the retina among Control (CON), EAU, ART-treated, and LCN2-inhibitor groups. (A, D) Quantification of FTH1 protein expression. (B, E) Quantification of GPX4 protein levels. (C, F) Quantification of SLC7A11 protein expression. (G) Representative images of ROS immunofluorescence staining (60× magnification). (H) Mean immunofluorescence intensity of ROS. (I) Retinal SOD activity among the groups. n = 3. ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Expressing, Control, Immunofluorescence, Staining, Activity Assay

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Immunofluorescence co-staining of microglia, astrocytes, and LCN2 in the retina. (A) Representative images of GFAP (astrocyte marker, white arrows) and LCN2 (red arrows) co-staining in Control (CON) and EAU groups (20× magnification). Magnified merged images (100×). (B) Representative images of IBA1 (microglial marker, white arrows), LCN2 (red arrows), and their co-localization (yellow arrows) among CON, EAU, ART-treated, and LCN2-inhibitor groups (20× magnification). Magnified merged images (100×). (C, E) Relative protein expression of the microglial marker IBA1. (D, F) Relative protein expression of the M1 microglial marker iNOS. n = 3. ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Immunofluorescence, Staining, Marker, Control, Expressing

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Effects of ART and si-LCN2 on LCN2 Expression in BV2 Cells. (A) CCK-8 assay for BV2 cell viability. The graph shows the viability of BV2 cells following treatment with various concentrations of ART (0, 0.1, 1, 10 µM). (B, E) Relative protein expression of LCN2 under different concentrations of ART (0, 0.1, 1, 10 μM). (C, F) Relative protein expression of LCN2 in BV2 cells 24 h after transfection with si-NC or si-LCN2. (D, G) Relative protein expression of LCN2 in BV2 cells among Control (CON), LPS, LPS+1 μM ART, and LPS + si-LCN2 groups. Data are shown as mean ± SD (n = 3). ns (not significant), ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Expressing, CCK-8 Assay, Transfection, Control

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Inflammatory cytokine profile in BV2 cells across Control (CON), LPS, LPS+1 µM ART, and LPS + si-LCN2 groups. (A-F) Protein levels of IL-1β, IL-6, and TNF-α were determined by Western blot. (G-I) Secreted cytokine concentrations were quantified by ELISA. n = 3. ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Control, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Redox Report : Communications in Free Radical Research

Article Title: Artesunate ameliorates experimental autoimmune uveitis by inhibiting the LCN2-STAT3 axis and suppressing microglial activation

doi: 10.1080/13510002.2026.2627096

Figure Lengend Snippet: Molecular mechanism of ART and the LCN2 inhibitor. (A)Representative images of IL17A (white arrows) and CD4 (CD4 + cell marker, red arrows) and their co-localization (yellow arrows) among CON, EAU, ART-treated, and LCN2-inhibitor groups (20× magnification). Magnified merged images (100×). (B, E) Relative protein expression of IL17A in the retina among Control (CON), EAU, ART-treated, and LCN2-inhibitor groups. (C, F) Relative protein expression of STAT3 in the retina among groups. (D, G) Relative protein expression of phosphorylated STAT3 (p-STAT3) in the retina among groups. n = 3. ** P < 0.01.

Article Snippet: LCN2 (MedChemExpress, HY-P70658A) was diluted to 50 μg/mL in immobilization buffer and immobilized on flow cell 3 (Fc3), resulting in approximately 5500 response units (RU).

Techniques: Marker, Expressing, Control

Journal: bioRxiv

Article Title: The RNA-binding protein Imp1 promotes a Spdef transcriptional program and mucus fucosylation during necrotizing enterocolitis

doi: 10.64898/2026.01.30.702645

Figure Lengend Snippet: A) Gross images of intestine from dam-fed and NEC mice. Putative pneumatosis is indicated by arrows. B) Cytokine gene expression for Il1b and Lcn2 was assessed in whole-thickness intestine using qRT-PCR in Imp1 IEC-OE versus wild-type dam-fed and NEC mice. Each data point represents one animal, n=30-31 mice per group. The data are not normally distributed and were therefore analyzed using the Mann-Whitney test. Error bars represent the SEM, * P <0.05. C) NEC mice exhibit epithelial vacuolization and damage assessed by hemotoxylin & eosin (H&E) staining and scored D) by a pathologist blinded to animal genotype and treatment. Scores were assigned as follows: 0 = no abnormality; 1 = mild vacuolization; 2 = full-thickness vacuolization; 3 = vacuolization with basal detachment of epithelium. Each dot represents one animal, n = 12-16 mice per group. Data were analyzed by a 2-way ANOVA with Tukey’s test for multiple comparisons. Error bars represent the SEM and * P <0.05 was considered statistically significant.

Article Snippet: Mouse : insulin-like growth factor 2 mRNA binding protein (Igf2bp1, Mm00501602_m1), interleukin 1 beta (Il1B, Mm00434228_m1), lipocalin 2 (LCN2, Mm01324470_m1), hypoxanthine guanine phosphoribosyl transferase (Hprt, Mm03024075_m1).

Techniques: Gene Expression, Quantitative RT-PCR, MANN-WHITNEY, Staining

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: Transcriptome results showed that genes such as LCN2 and C1q were significantly upregulated in the hippocampus. A Volcano plot of differentially expressed genes (DEGs) in hippocampus from silica-exposed (Sil) versus vehicle (Veh) mice. Cut-off: \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\:\left|{log}_{2}FC\right|\geqq\:O.O5$$\end{document} , \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\:Pvalue\leqq\:0.05$$\end{document} , indicated by gray dashed lines in the plot. Red, significantly up-regulated; blue, significantly down-regulated; grey, non-significant. n = 3 biological replicates per group. B Gene set enrichment analysis of the 2,275 up-regulated genes using the Metascape database. C Inflammatory module network analysis of the DEGs enriched in GO:0006954 (GO database), circled by red in ( B ). D Neutrophil degranulation cascade module network analysis of the DEGs enriched in R-MMU-6,798,695 (Reactome database), circled by green in ( B ). E Microglial phagocytosis module network analysis of the DEGs enriched in WP3626 (WikiPathways database), circled by yellow in ( B ). F LCN2 and complement receptor C3ar1 were identified as having potential interactions. Interactions between genes among C-F are indicated by lines, whose colors represent interaction types from STRING database

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques:

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: LCN2 further activates microglia, exacerbating neuroinflammation in the hippocampus. A Representative immunohistochemical staining of LCN2 in the CA1, CA3, and DG regions of paraffin-embedded tissue from Veh and Sil groups; scale bar: 50 μm. The black arrow indicates LCN2-positive cells, brown DAB precipitate indicates positive immunoreactivity. B Quantitative analysis of positive staining from panel A, ( n = 4). C Western blot analysis assessing LCN2 protein expression. D LCN2 expression levels in Veh and Sil group mice ( n = 9). E Representative images of LCN2 immunoreactivity (green) and Iba-1 (red) in the CA1, CA3, and DG regions of frozen tissue from Veh and Sil groups; scale bar: 50 μm. F Representative immunofluorescence images of frozen sections showing Iba-1-positive cells (red); scale bar: 50 μm. G Sholl analysis of microglia in frozen tissue from Veh and Sil groups, measuring the distance from the soma (in 2 μm increments) and the number of microglial processes intersecting concentric circles ( n = 4). Maxima for all measures were observed approximately 20 μm from the soma. Data are presented as mean ± SEM. For panels ( B ) and ( D ), data were analyzed by t-tests. For panel ( G ), data were analyzed by two-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns = not significant

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques: Immunohistochemical staining, Staining, Western Blot, Expressing, Immunofluorescence

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: LCN2 activates microglia through the MC4R receptor rather than the MC1R or MC3R receptors in the hippocampus. A Western blot analysis assessing MC4R, MC1R, and MC3R protein expression. B Protein expression (normalized to β-actin) of MC4R, MC1R, and MC3R in tissue from Veh and Sil group mice ( n = 9). C Representative images of MC4R immunoreactivity (green), LCN2 immunoreactivity (red), and Iba-1 (purple) in frozen tissue. Scale bar: 50 μm. D Quantitative analysis of the MC4R-positive cells of CA1, CA3, and DG regions ( n = 4). E Quantitative analysis of the LCN2-positive cells of CA1, CA3, and DG regions ( n = 4). F Quantitative analysis of the MC4R + LCN2 + Iba-1 + cells (cell/mm 2 ) in the CA1, CA3, and DG regions ( n = 4). Data are presented as mean ± SEM. For panels (B-C, E-F), data were analyzed by t-tests. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns = not significant

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques: Western Blot, Expressing

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: LCN2-mediated cAMP/PKA/NF-κB signaling and C1q upregulation, with HS024 inhibiting C1q release in the BV2 cell culture. A ELISA measurement of cAMP in cell culture supernatant ( n = 4). The main effects of LCN2 (F = 92.206, p < 0.001) and HS024 (F = 18.470, p = 0.001) were both significant. B Western blot analysis assessing the expression levels of MC4R, PKA, NF-κB p65, and C1q in four groups. C Quantitative analysis of MC4R protein expression (normalized to β-actin) ( n = 3). The main effects of LCN2 (F = 6.863, p = 0.031) and HS024 (F = 17.455, p = 0.003) were significant. D Quantitative analysis of PKA protein expression (normalized to GAPDH) ( n = 3). The main effects of LCN2 (F = 15.842, p = 0.004) was significant; HS024 (F = 3.303, p = 0.107) was not. E Quantitative analysis of phosphorylated P65 (P-P65) protein expression (normalized to total P65) ( n = 3). The main effect of HS024 (F = 11.158, p = 0.010) was significant; LCN2 (F = 3.929, p = 0.083) was not. F Quantitative analysis of C1q protein expression (normalized to GAPDH) ( n = 3). The main effects of LCN2 (F = 14.909, p = 0.005) was significant; HS024 (F = 1.731, p = 0.225) was not. G Immunofluorescence analysis after conditional treatment. Representative images of P65 immunoreactivity (green) and DAPI nuclear staining (blue) in BV-2 cells. White arrows indicate P65 nuclear expression-positive cells. H Quantitative analysis of the results in G, ( n = 4). Scale bar: 50 μm. The main effects of LCN2 (F = 12.917, p = 0.004) was significant; HS024 (F = 2.696, p = 0.127) was not. I ELISA measurement of C1q in cell culture supernatant ( n = 4). The main effects of LCN2 (F = 37.783, p < 0.001) and HS024 (F = 9.739, p = 0.009) were both significant. J Western blot analysis to assess the expression levels of TNF-α and TGF-β in four groups. K Quantitative analysis of TNF-α protein expression (normalized to GAPDH) ( n = 3). The main effects of LCN2 (F = 22.812, p = 0.001) and HS024 (F = 96.627, p < 0.001) were both significant. L Quantitative analysis of TGF-β protein expression (normalized to GAPDH) ( n = 3). The main effect of HS024 (F = 65.778, p < 0.001) was significant; LCN2 (F = 0.994, p = 0.348) was not. Data are presented as mean ± SEM. For panels ( A , C - F , H - I , K - L ), data were analyzed by two-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns = not significant

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques: Cell Culture, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Staining

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: PF ameliorates neuronal loss induced by silica exposure, which is accompanied by anxiety- and depression-like behaviors in the hippocampus. A Representative activity traces of mice in the OFT across four groups. B Total distance traveled by mice in the OFT ( n = 8). The main effects of Sil (F = 20.072, p < 0.001) and PF (F = 0.637, p = 0.432). C Immobility time in the OFT ( n = 8). The main effects of Sil (F = 20.513, p < 0.001) and PF (F = 5.440, p = 0.027). D Time spent in the central area of the OFT ( n = 8). The main effects of Sil (F = < 0.001, p = 0.983) and PF (F = 0.527, p = 0.474). E Activity trajectories of mice in the open arms and closed arms of the EPM. The red arrow indicates open arms; the green arrow indicates closed arms. F Total distance traveled by mice in the EPM ( n = 8). The main effects of Sil (F = 1.024, p = 0.320) and PF (F = 2.498, p = 0.125). G Time spent in the open arms ( n = 8). The main effects of Sil (F = 1.157, p = 0.291) and PF (F = 5.258, p = 0.030). H Number of entries into the open arms ( n = 8). The main effects of Sil (F = 8.321, p = 0.007) and PF (F = 0.771, p = 0.387). I Number of marbles buried by mice in the MBT ( n = 8). The main effects of Sil (F = 6.215, p = 0.019) and PF (F = 0.559, p = 0.461). J Western blot analysis assessing the expression levels of LCN2, MC4R, C1q, and BDNF in the four groups of mice. K Quantitative analysis of LCN2 protein expression ( n = 9). The main effects of Sil (F = 2.801, p = 0.104) and PF (F = 8.961, p = 0.005). L Quantitative analysis of MC4R protein expression ( n = 9). The main effects of Sil (F = 22.590, p < 0.001) and PF (F = 9.298, p = 0.005). M Quantitative analysis of C1q protein expression ( n = 9). The main effects of Sil (F = 5.380, p = 0.027) and PF (F = 65.328, p < 0.001). N Quantitative analysis of BDNF protein expression ( n = 9). The main effects of Sil (F = 18.296, p < 0.001) and PF (F = 24.246, p < 0.001). Data are presented as mean ± SEM. For panels (B-D, F-I, K-N), data were analyzed by two-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns = not significant

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques: Activity Assay, Western Blot, Expressing

Journal: Journal of Neuroinflammation

Article Title: A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release

doi: 10.1186/s12974-026-03695-5

Figure Lengend Snippet: Proposed mechanism by which the microglial LCN2-MC4R signaling axis drives silica-induced neuronal loss. Silica exposure in the lungs triggers the release of LCN2. Both LCN2 and TNF-α then travel to the hippocampus, cross the blood-brain barrier, and activate microglia. In microglia, LCN2 binds to the MC4R, activating the cAMP/PKA/NF-κB signaling pathway. This activation stimulates microglia to release C1q, which initiates the complement cascade, leading to C3 deposition on neurons. These C3-tagged neurons are subsequently targeted by microglia, resulting in neuronal loss

Article Snippet: Cells were cultured in medium containing LCN2 (Sino Biological, 50409-M08H) at 100 ng/ml, the MC4R antagonist HS024 (MedChem Express, HY-P1215A) at 100 nM, or a combination of LCN2 and HS024 (LCN2-HS024) for 24 h. Cell supernatants were collected for subsequent ELISA analysis.

Techniques: Activation Assay