neuraminidase p2988  (MedChemExpress)

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: Neuraminidase activity is upregulated in vivo and in vitro following ischemic injury. (A) Neuraminidase activity in pig serum after CA/CPR, measured at post‐ROSC 0.5, 6, 12, and 24 h. (B) Neuraminidase activity in BV2 microglial cell culture supernatant following oxygen–glucose deprivation/reperfusion (OGD/R), assessed at 0, 12, 24, and 48 h postreperfusion. Both models exhibited a time‐dependent upward trend in neuraminidase activity, peaking at post‐ROSC 24 h (serum) and 48 h (cell supernatant). Data are reported as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. BL/Control group (two‐way ANOVA with Bonferroni post hoc test).

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: Activity Assay, In Vivo, In Vitro, Cell Culture, Control

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: OP enhances microglial viability and preserves α2,6‐sialic acid expression in BV2 cells following OGD/R. (A) Cell viability of BV2 microglia treated with increasing OP concentrations (0–180 μM) at 24 h and 48 h post‐OGD/R, assessed using the Cell Counting Kit‐8 (CCK‐8) assay. Data are presented as mean ± SEM. ** p < 0.01, *** p < 0.001 vs. 24/48 h untreated group. ### p < 0.001 vs. 40 μM OP to 48 h group (two‐way ANOVA with Bonferroni post hoc test). (B) α2,6‐linked sialic acid expression on BV2 microglia surface, evaluated by SNA‐FITC fluorescence staining (green) and flow cytometry. Representative fluorescent images (40× magnification) show SNA‐FITC signal intensity. Nuclei (blue) counterstained with DAPI. Scale bar: 20 μm. (C) Flow cytometry was used to assess the levels of α2,6‑sialylation in the different treatment groups. NA, neuraminidase; OP, oseltamivir phosphate.

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: Expressing, Cell Counting, CCK-8 Assay, Fluorescence, Staining, Flow Cytometry

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: OP inhibits in vitro neuraminidase‐mediated NF‐κB pathway activation. (A) Immunofluorescence images showing NF‐κB p65 subcellular localization in BV2 microglia. Nuclei are stained with DAPI (blue), p65 is labeled with an anti‐p65 antibody (red), and merged images highlight nuclear translocation. Scale bar: 20 μm. (B) Quantification of cytoplasmic/nuclear p65 ratio in control, OGD/R, OGD/ R + OP (40 μM), and OGD/ R + NA (12.5 U/mL). Data expressed as a percentage of nuclear p65 distribution. (C, D) Representative Western blot (C) and quantitative analysis (D) of total NF‐κB p65, p‐NF‐κB p65 (Ser536), and Lamin‐B1, with β‐Tublin used as internal controls for nuclear and cytosolic fractions, respectively. Quantifications of p‐IκBα (Ser32/36), TNF‐α, and HMGB1 protein expression, normalized to total IκBα, and β‐Tubulin. (E) ELISA quantification of secreted HMGB1, IL‐6, and TNF‐α in BV2 microglial supernatants. NA, Neuraminidase. Values represent mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 (one‐way ANOVA with Bonferroni post hoc test).

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: In Vitro, Activation Assay, Immunofluorescence, Staining, Labeling, Translocation Assay, Control, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: OP preserves CD24‐Siglec‐G/10 interaction by counteracting neuraminidase‐mediated desialylation. (A) Co‐immunoprecipitation (Co‐IP) and Western blot analysis of CD24 and Siglec G interactions in BV2 microglia in control, OGD/R, OGD/ R + OP (40 μM), and Control + NA (12.5 U/mL). Lysates were immunoprecipitated with anti‐CD24 antibody and probed for Siglec‐G. Quantification of Siglec‐G and CD24 binding ratios normalized to untreated controls. (B) Dual immunofluorescence staining of CD24 (red) and Siglec‐G (green) localization in BV2 microglia. Nuclei are counterstained with DAPI (blue). Merged images demonstrate CD24‐Siglec‐G co‐localization (yellow). Scale bar: 10 μm. (C) Quantification of CD24‐Siglec‐G co‐localization using Pearson's correlation coefficient ( r ). NA, Neuraminidase. Data represent mean ± SEM. * p < 0.05, ** p < 0.01 (one‐way ANOVA with Bonferroni post hoc test).

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: Immunoprecipitation, Co-Immunoprecipitation Assay, Western Blot, Control, Binding Assay, Immunofluorescence, Staining

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: CD24 and Siglec‐G overexpression attenuates neuroinflammatory signaling in OGD/R‐injured BV2 microglia. (A) Representative western blotting bands of Siglec‐G, CD24, p‐NF‐κB‐p65 (Ser536), NF‐κB p65, p‐IκBα (Ser32/36), IκBα, TNF‐α, and HMGB protein levels in BV2 cells subjected to CD24/Siglec‐G silencing (siRNA) or overexpression (pcDNA3.1(+)) followed by OGD/R. (B) Quantitative analysis of Siglec‐G and CD24 protein levels normalized to β‐tubulin. (C) Cytoplasmic and nuclear p65 phosphorylation levels quantified as the ratio of phosphorylated to total p65. Nuclear fractions normalized to Lamin‐B1; cytoplasmic fractions normalized to β‐tubulin. (D) Quantification of p‐IκBα, total IκBα, TNF‐α, and HMGB1 protein expression normalized to β‐tubulin. (E) Immunofluorescence images illustrating NF‐κB p65 subcellular localization. Nuclei are stained with DAPI (blue), p65 is labeled with an anti‐p65 antibody (red), and merged images highlight nuclear translocation. Scale bar: 20 μm. (F) Quantification of cytoplasmic/nuclear p65 ratio in control, OGD/R, OGD/R+si‐ CD24‐Siglec‐G , and OGD/R+ pcDNA3.1(+)‐ CD24‐Siglec‐G . Nuclear p65 distribution data presented as percentages. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 (one‐way ANOVA with Bonferroni post hoc test).

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: Over Expression, Western Blot, Phospho-proteomics, Expressing, Immunofluorescence, Staining, Labeling, Translocation Assay, Control

Journal: CNS Neuroscience & Therapeutics

Article Title: Oseltamivir Phosphate Modulates CD24 ‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest

doi: 10.1111/cns.70495

Figure Lengend Snippet: OP modulates NF‐κB pathway activity via the CD24‐Siglec‐G/10 axis in BV2 microglia. (A, B) Western blot (A) and quantitative analysis (B) of Siglec‐G and CD24 protein expressions in CD24/Siglec‐G‐silenced BV2 cells treated with OP (40 μM) following OGD/R. Protein levels normalized to β‐tubulin. (C, D) Cytoplasmic and nuclear p65 phosphorylation levels quantified as the ratio of phosphorylated to total p65. Nuclear fractions normalized to Lamin‐B1; cytoplasmic fractions normalized to β‐tubulin. (E–G) Western blot and relative quantification of p‐IκBα (Ser32/36), TNF‐α, and HMGB1 proteins, normalized to total IκBα and β‐tubulin. Values represent mean ± SEM, * p < 0.05, ** p < 0.01 (two‐way ANOVA with Bonferroni post hoc test).

Article Snippet: During OGD/R, α2,6‐linked sialic acid residues were removed from the BV2 cell surface after 12.5 U/mL neuraminidase (HY‐P2988, MCE) treatment, as previously described [ ].

Techniques: Activity Assay, Western Blot, Phospho-proteomics, Quantitative Proteomics

Journal: RSC Advances

Article Title: MedChemExpress compounds prevent neuraminidase N1 via physics- and knowledge-based methods †

doi: 10.1039/d4ra02661f

Figure Lengend Snippet: The data from docking simulations and experiments of known inhibitors against N1 neuraminidase a

Article Snippet: MedChemExpress compounds prevent neuraminidase N1 via physics- and knowledge-based methods.

Techniques: