non-contact spotting robot sciflexarrayer s3 Search Results


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SCIENION noncontact microarray printer
<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Noncontact Microarray Printer, supplied by SCIENION, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SCHOTT nhs-activated nexterion® slides
<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Nhs Activated Nexterion® Slides, supplied by SCHOTT, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Amine Reactive, Nhs Activated Glass Slides (Nexterion ® Slide H, supplied by SCHOTT, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Nexterion H Functionalized Glass Slides, supplied by SCHOTT, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Activated Glass Slides Nexterion Slide H, supplied by SCHOTT, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Tekdon Inc masked-well glass slides coated teflon/epoxy-silane
<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Masked Well Glass Slides Coated Teflon/Epoxy Silane, supplied by Tekdon Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Nexterion Slide H, supplied by SCHOTT, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
Rabbit Anti Ebov Vlp Polyclonal Antibodies, supplied by IBT Bioservices, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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<t>Microarray</t> analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D
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Image Search Results


Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D

Journal: Journal of Neuroinflammation

Article Title: Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection

doi: 10.1186/s12974-025-03482-8

Figure Lengend Snippet: Microarray analysis reveals the effects of GFAP mAb treatment on key inflammatory mediators in glaucomatous retina. ( A - C ) The expression of TLR4 and S100A8 was significantly downregulated by 25–50 µg GFAP mAb treatment compared to the vehicle. The marker for microglial activation, CD68, was significantly decreased in the 25 µg GFAP mAb treatment group. ( D - F ) Proteins of the inflammasome pathway, NLRP3, GSDMD and Caspase-1 were significantly downregulated in the 25 µg GFAP mAb treatment group. With the 50 µg dose, these protein expressions showed a similar downward trend, but without statistical significance. ( G ) Expression profiling of inflammation-associated mediators showed that 25 µg GFAP mAb significantly decreased pro-inflammatory factors (TNF-α, IL-1β, IL-8, MMP9, and IFN-γ), and increased the anti-inflammatory cytokine IL-10 compared to the vehicle group. In contrast, the 50 µg dose significantly reduced IFN-γ only. ( H ) Representative images of spots showing IL-1β levels in the subarrays for each group. Image analysis was conducted with Imagene software, using the median intensity from each spot to calculate the mean of the triplicate spots for each marker. For CD68 and TLR4, due to significant heterogeneity in SDs, statistical analysis was performed using Welch’s ANOVA followed by the Tamhane T2 post hoc test. All other data were analyzed using one-way ANOVA with Tukey’s post hoc test. Data are presented as the mean ± SD; n = 4 per group; * p < 0.05, ** p < 0.01, *** p < 0.001; ns = not significant. TLR4 – Toll-Like Receptor 4. S100A8 – S100 Calcium Binding Protein A8. NLRP3 – NLR Family Pyrin Domain Containing 3. GSDMD – Gasdermin D

Article Snippet: Briefly, the microarray was prepared using a noncontact microarray printer (SciFLEXARRAYER S3; Scienion, Berlin, Germany).

Techniques: Microarray, Expressing, Marker, Activation Assay, Software, Binding Assay