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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes <t>CXCL5</t> secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.
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Effect of B. coagulans spores, PSCF and synbiotic on immune markers in colon tissues and blood serum. Protein levels of cytokines including ( A ) IL-1α, ( B ) IL-1β, ( C ) IL-6, ( D ) IL-12, ( E ) TNF-α, ( F ) IFN-γ in proximal and distal colon explants as well as cytokine levels of ( G ) IL-1β, ( H ) IL-10, and ( I ) IL-12 in blood serum were analysed by Bio-plex. iNOS activity in colon tissues ( J ) measured by NOS activity assay and CRP levels in serum ( K ) by <t>ELISA.</t> Statistical significance among groups evaluated by one-way ANOVA followed by Tukey’s test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. DSS-colitic group and data expressed as mean ± SEM ( n = 3 per group).
Mouse C Reactive Protein Crp Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 4 Transcriptomes of HMCs and HRPCs in response to control or AGEs treatment. a The overlap of highly expressed genes in the normal control groups of HMCs and HRPCs. b Shared enriched GO pathways between HMCs and HRPCs, sorted by p-value. c Volcano plot shows DEGs in HMCs and HRPCs treated with AGEs. The red dots indicate upregulated genes while blue dots indicate downregulated genes. d Expression levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 and CXCL8 were measured by real-time PCR and <t>ELISA</t> between control and AGEs groups. e Significantly enriched KEGG pathways of DEGs in both HMCs and HRPCs treated with AGEs, the size of circle represents genes number enriched in pathways, the darker color of circle indicates a smaller p-value. f The chemokine scores of MCs and RPCs in wt and db/db mice. g The proportions of infiltrating neutrophils and macrophages in the glomeruli of wt and db/db mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
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Fig. 4 Transcriptomes of HMCs and HRPCs in response to control or AGEs treatment. a The overlap of highly expressed genes in the normal control groups of HMCs and HRPCs. b Shared enriched GO pathways between HMCs and HRPCs, sorted by p-value. c Volcano plot shows DEGs in HMCs and HRPCs treated with AGEs. The red dots indicate upregulated genes while blue dots indicate downregulated genes. d Expression levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 and CXCL8 were measured by real-time PCR and <t>ELISA</t> between control and AGEs groups. e Significantly enriched KEGG pathways of DEGs in both HMCs and HRPCs treated with AGEs, the size of circle represents genes number enriched in pathways, the darker color of circle indicates a smaller p-value. f The chemokine scores of MCs and RPCs in wt and db/db mice. g The proportions of infiltrating neutrophils and macrophages in the glomeruli of wt and db/db mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
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Fig. 4 Transcriptomes of HMCs and HRPCs in response to control or AGEs treatment. a The overlap of highly expressed genes in the normal control groups of HMCs and HRPCs. b Shared enriched GO pathways between HMCs and HRPCs, sorted by p-value. c Volcano plot shows DEGs in HMCs and HRPCs treated with AGEs. The red dots indicate upregulated genes while blue dots indicate downregulated genes. d Expression levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 and CXCL8 were measured by real-time PCR and <t>ELISA</t> between control and AGEs groups. e Significantly enriched KEGG pathways of DEGs in both HMCs and HRPCs treated with AGEs, the size of circle represents genes number enriched in pathways, the darker color of circle indicates a smaller p-value. f The chemokine scores of MCs and RPCs in wt and db/db mice. g The proportions of infiltrating neutrophils and macrophages in the glomeruli of wt and db/db mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
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Image Search Results


Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes CXCL5 secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: Cell death & disease

Article Title: Cancer-derived exosomal HSPC111 promotes colorectal cancer liver metastasis by reprogramming lipid metabolism in cancer-associated fibroblasts.

doi: 10.1038/s41419-022-04506-4

Figure Lengend Snippet: Fig. 6 An increase in levels of acetyl-CoA and H3K27ac promotes CXCL5 secretion in CAFs. The effects of acetate treatment on acetyl-CoA levels in LX-2 cells incubated with ExoHCT116 (A) and ExoSW480 (B). Western blot showed the effects of acetate treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 (C) and ExoSW480 (D). E The effects of Trichostatin A (TSA) treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoHCT116 KD and their relative control. F The effects of C646 treatment on CXCL5 and H3K27ac levels in LX-2 cells incubated with ExoSW480 OE and their relative control. G, H Chromatin immunoprecipitation (ChIP) assays using IgG as a control were performed with antibody against H3K23ac. Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl or in LX-2 cells incubated with ExoHCT116 KD and ExoHCT116 KD Ctrl and treated with TSA (G). Examination of H3K27 acetylation status in CXCL5 gene promoter region in LX-2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl or in LX- 2 cells incubated with ExoSW480 OE and ExoSW480 OE Ctrl and treated with C646 (H). Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Cells were cultured in the presence of appropriate exosomes (20μg/mL) for 48 h before supernatants were collected, and the CXCL5 level was detected by CXCL5 ELISA kit (EK0728, BOSTER) according to the manufacturer’s protocols.

Techniques: Incubation, Western Blot, Control, Chromatin Immunoprecipitation

Fig. 8 A schematic diagram of mechanism of exosomal HSPC111 facilitates CRLM via reprogramming lipid metabolism in CAFs. Exosomal HSPC111 derived from CRC cells phosphorylates ACLY in CAFs, leading to the increased levels of acetyl-CoA and histone acetylation to secrete CXCL5, and resulting in CRC cells colonized in liver via the CXCL5-CXCR2 axis.

Journal: Cell death & disease

Article Title: Cancer-derived exosomal HSPC111 promotes colorectal cancer liver metastasis by reprogramming lipid metabolism in cancer-associated fibroblasts.

doi: 10.1038/s41419-022-04506-4

Figure Lengend Snippet: Fig. 8 A schematic diagram of mechanism of exosomal HSPC111 facilitates CRLM via reprogramming lipid metabolism in CAFs. Exosomal HSPC111 derived from CRC cells phosphorylates ACLY in CAFs, leading to the increased levels of acetyl-CoA and histone acetylation to secrete CXCL5, and resulting in CRC cells colonized in liver via the CXCL5-CXCR2 axis.

Article Snippet: Cells were cultured in the presence of appropriate exosomes (20μg/mL) for 48 h before supernatants were collected, and the CXCL5 level was detected by CXCL5 ELISA kit (EK0728, BOSTER) according to the manufacturer’s protocols.

Techniques: Derivative Assay

Effect of B. coagulans spores, PSCF and synbiotic on immune markers in colon tissues and blood serum. Protein levels of cytokines including ( A ) IL-1α, ( B ) IL-1β, ( C ) IL-6, ( D ) IL-12, ( E ) TNF-α, ( F ) IFN-γ in proximal and distal colon explants as well as cytokine levels of ( G ) IL-1β, ( H ) IL-10, and ( I ) IL-12 in blood serum were analysed by Bio-plex. iNOS activity in colon tissues ( J ) measured by NOS activity assay and CRP levels in serum ( K ) by ELISA. Statistical significance among groups evaluated by one-way ANOVA followed by Tukey’s test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. DSS-colitic group and data expressed as mean ± SEM ( n = 3 per group).

Journal: Nutrients

Article Title: Synbiotic Supplementation Containing Whole Plant Sugar Cane Fibre and Probiotic Spores Potentiates Protective Synergistic Effects in Mouse Model of IBD

doi: 10.3390/nu11040818

Figure Lengend Snippet: Effect of B. coagulans spores, PSCF and synbiotic on immune markers in colon tissues and blood serum. Protein levels of cytokines including ( A ) IL-1α, ( B ) IL-1β, ( C ) IL-6, ( D ) IL-12, ( E ) TNF-α, ( F ) IFN-γ in proximal and distal colon explants as well as cytokine levels of ( G ) IL-1β, ( H ) IL-10, and ( I ) IL-12 in blood serum were analysed by Bio-plex. iNOS activity in colon tissues ( J ) measured by NOS activity assay and CRP levels in serum ( K ) by ELISA. Statistical significance among groups evaluated by one-way ANOVA followed by Tukey’s test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. DSS-colitic group and data expressed as mean ± SEM ( n = 3 per group).

Article Snippet: The levels of C-reactive protein (CRP) in serum from respective groups ( n = 3 samples/group) were analysed using Mouse C-Reactive Protein/CRP Quantikine Elisa kit (MCRP00, R and D Systems, Australia) following the manufacturer’s instructions.

Techniques: Activity Assay, Nos Activity Assay, Enzyme-linked Immunosorbent Assay

Fig. 4 Transcriptomes of HMCs and HRPCs in response to control or AGEs treatment. a The overlap of highly expressed genes in the normal control groups of HMCs and HRPCs. b Shared enriched GO pathways between HMCs and HRPCs, sorted by p-value. c Volcano plot shows DEGs in HMCs and HRPCs treated with AGEs. The red dots indicate upregulated genes while blue dots indicate downregulated genes. d Expression levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 and CXCL8 were measured by real-time PCR and ELISA between control and AGEs groups. e Significantly enriched KEGG pathways of DEGs in both HMCs and HRPCs treated with AGEs, the size of circle represents genes number enriched in pathways, the darker color of circle indicates a smaller p-value. f The chemokine scores of MCs and RPCs in wt and db/db mice. g The proportions of infiltrating neutrophils and macrophages in the glomeruli of wt and db/db mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Journal: Communications biology

Article Title: Single-cell transcriptomes reveal a molecular link between diabetic kidney and retinal lesions.

doi: 10.1038/s42003-023-05300-4

Figure Lengend Snippet: Fig. 4 Transcriptomes of HMCs and HRPCs in response to control or AGEs treatment. a The overlap of highly expressed genes in the normal control groups of HMCs and HRPCs. b Shared enriched GO pathways between HMCs and HRPCs, sorted by p-value. c Volcano plot shows DEGs in HMCs and HRPCs treated with AGEs. The red dots indicate upregulated genes while blue dots indicate downregulated genes. d Expression levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 and CXCL8 were measured by real-time PCR and ELISA between control and AGEs groups. e Significantly enriched KEGG pathways of DEGs in both HMCs and HRPCs treated with AGEs, the size of circle represents genes number enriched in pathways, the darker color of circle indicates a smaller p-value. f The chemokine scores of MCs and RPCs in wt and db/db mice. g The proportions of infiltrating neutrophils and macrophages in the glomeruli of wt and db/db mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Chemokines in the cell culture supernatant were assayed using enzyme-linked immunosorbent assay (ELISA) kits (EK0722, EK0728, EK0359 and EK0413 from BOSTER, Wuhan, China and EK1264 and EK1265 from MULTI SCIENCES, Hangzhou, China) following the manufacturer’s instructions.

Techniques: Control, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay