nop2  (Proteintech)

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: S100B−/− mice had improved retention memory function after traumatic brain injury (TBI). (A) TBI induced sensorimotor impairments at all time points when compared with sham-injured mice in the beam walk test (***P<0.001, **P<0.01, vs. sham). However, S100B−/− mice failed to show any improvement in sensorimotor function. Analysis by repeated measures two-way analysis of variance (ANOVA) followed by Tukey's post-hoc test. (B) S100B−/− mice showed significant improvement (+P<0.05, vs. S100B+/+) in Discrimination Index in the novel object recognition task. Analysis by one-way ANOVA followed by Tukey's post-hoc test. (Mean±s.e.m.; n=11 to 14/group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques:

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: S100B−/− mice had reduced lesion volume but no reduction in neuronal cell loss after traumatic brain injury (TBI). (A) Histologic assessment using unbiased stereology showed that S100B+/+ mice developed a large lesion following TBI, whereas S100B−/− mice showed a significant reduction in lesion size (*P<0.05, vs. S100B+/+). Analysis by one-tailed unpaired Student's t-test. (B) Representative images of the cresyl violet-stained sections show the reduction in lesion volume observed in S100B−/− samples. Stereological assessment of surviving neurons using unbiased stereological techniques was performed in the cortex (C), thalamus (D), and cornu ammonis 1 (CA1) (E) subregion of the hippocampus at 28 days after injury. TBI resulted in significant neuronal cell loss in the cortex (*P<0.05, vs. sham), thalamus (*P<0.05 or **P<0.01, vs. sham), and CA1 hippocampal subregion (**P<0.01, vs. sham). S100B−/− mice did not show any improvement in neuronal survival in all the assessed brain regions. Analysis by one-way analysis of variance followed by Tukey's post-hoc test. (Mean±s.e.m.; n=4 to 7/group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: One-tailed Test, Staining

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: S100B−/− mice had reduced microglial activation in the injured cortex after traumatic brain injury (TBI). Stereological assessment of microglial cell number and activation phenotype was performed in the cortex at 7 and 28 days after TBI. (A) Representative images of the Iba-1-stained sections show morphologic features of ramified and hypertrophic and bushy (activated) microglia. (B) S100B−/− mice showed statistically significant increases in the numbers of ramified microglia on 28 days after injury (**P<0.01, vs. sham; +P<0.05, vs. S100B+/+, #P<0.05, vs. S100B−/− at 7 days) when compared with sham and S100B+/+ mice (at 28 days) and S100B−/− mice at 7 days. TBI resulted in significant microglial activation at 7 days after injury (*P<0.05, vs. sham) followed by sustained increases in numbers of activated microglia at 28 days (***P<0.001, vs. sham) when compared with sham. S100B−/− mice showed significant attenuation in the numbers of activated microglia at 28 days (+P<0.05, vs.S100B+/+) when compared with S100B+/+ mice. Analysis by one-way analysis of variance followed by Tukey's post-hoc test. (Mean±s.e.m.; n=4 to 7/group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: Activation Assay, Staining

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: Systemic administration of a neutralizing S100B antibody improved functional outcomes following traumatic brain injury (TBI). (A) TBI induced significant sensorimotor impairments at all time points when compared with sham-injured mice in the beam walk test (***P<0.001, vs. sham). Anti-S100B immunoglobulin G (IgG)-treated mice exhibited significant improvements in sensorimotor performance at 7, 14, 21, and 28 days (+P<0.05, vs. vehicle; ^P<0.05, vs. IgG control) after injury when compared with vehicle-treated and IgG control-treated mice. Analysis by repeated measures two-way analysis of variance (ANOVA) followed by Tukey's post-hoc test. (B) TBI-induced deficits in retention memory (P<0.001, vs. sham) in the novel object recognition task were significantly attenuated by systemic administration of anti-S100B IgG (++P<0.01, vs. vehicle); data expressed as Discrimination Index analysis by one-way ANOVA followed by Tukey's post-hoc test (mean±s.e.m.; n=8 to 14/injured group, n=6 to 7/sham group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: Functional Assay

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: Systemic administration of a neutralizing S100B antibody reduced lesion volume, improved neuronal survival, and attenuated microglial activation in the cortex after traumatic brain injury (TBI). (A) Histologic assessment using unbiased stereology showed that vehicle-treated mice developed a large lesion following TBI, whereas anti-S100B immunoglobulin G (IgG) treatment resulted in significant reduction in lesion size (***P<0.001, vs. vehicle). Systemic administration of IgG control significantly reduced the lesion volume (**P<0.01, vs. vehicle, +P<0.05, vs. anti-S100B IgG treatment). Analysis by one-way analysis of variance (ANOVA) followed by Tukey's post-hoc test (mean±s.e.m.; n=5 to 7/group). (B) Representative images of the cresyl violet-stained sections show the reduction in lesion volume observed in anti-S100B IgG-treated samples. (C) Stereological assessment of surviving neurons was performed using unbiased stereological techniques in the cortex at 28 days after injury. TBI resulted in significant neuronal cell loss in the cortex (**P<0.01, vs. sham). Systemic administration of anti-S100B IgG significantly improved neuronal survival in the cortex (+P<0.05, vs. vehicle) when compared with vehicle-treated samples. Analysis by one-way ANOVA followed by Tukey's post-hoc test (mean±s.e.m.; n=5/group). (D) Stereological assessment of microglial cell number and activation phenotype was performed in the cortex at 7 and 28 days after TBI. No statistically significant increases in the numbers of ramified microglia were observed on 7 and 28 days after injury. TBI resulted in significant and sustained increases in activated microglia at 7 days after injury followed by sustained increases at 28 days (***P<0.001, vs. sham). Systemic administration of anti-S100B IgG significantly attenuated microglial activation at 7 days after injury (+++P<0.001, vs. vehicle; (^^^P<0.001, vs. IgG control) when compared with vehicle- and IgG control-treated samples Furthermore, anti-S100B IgG continued to show significant reduction in the numbers of activated microglia at 28 days postinjury (+P<0.05, vs. vehicle) when compared with vehicle-treated samples. Analysis by one-way ANOVA followed by Tukey's post-hoc test (mean±s.e.m.; n=5/group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: Activation Assay, Staining

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: S100B–AGER complexes are not detectable in traumatic brain injury (TBI). Representative micrographs of ipsilateral cortical regions from TBI/sham sections 7 days after injury and positive/negative control sections processed for proximity ligation assays using S100B+AGER primary antibodies (brown) and counterstained with hematoxylin to visualize nuclei (blue).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: Negative Control, Ligation

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury

doi: 10.1038/jcbfm.2015.165

Figure Lengend Snippet: S100B does not influence microglial activation markers in vitro. Lipopolysaccharide (LPS) (A) and interferon-gamma (IFNγ) (B) stimulation in BV2 microglia significantly increased nitric oxide (NO) production at 24 h (***P<0.001, ****P<0.0001 vs. control). Pretreatment of cells with S100B (1 μm) did not significantly attenuate LPS- or IFNγ-stimulated increases in NO production. Analysis by one-way analysis of variance (ANOVA) followed by Tukey's post-hoc test (mean±s.d.; n=6/group). IFNγ stimulation in primary mouse microglia significantly increased NO (C) and reactive oxygen species (ROS) (D) production at 24 h (***P<0.001, ****P<0.0001 vs. control). Pretreatment of cells with S100B (1 μm) did not significantly attenuate IFNγ-stimulated increases in NO or ROS production. Analysis by one-way ANOVA followed by Tukey's post-hoc test (mean± s.d.; n=3/group).

Article Snippet: Neutralizing anti-S100B antibody treatment: Male C57Bl/6 mice (20 to 25 g, 3 months old) were randomized into six groups and administered 10 mg/kg anti-S100B (BL356, Bethyl Laboratories, Montgomery, TX, USA) or an isotype matched IgG (Catalog no. P50-1000, Bethyl Laboratories) antibody at 24 hours and 14 days after injury, via the intraperitoneal route, based on preliminary pharmacokinetic data.

Techniques: Activation Assay, In Vitro