Journal: Molecular and cellular endocrinology

Article Title: Estrogen receptor beta maintains expression of KLF15 to prevent cardiac myocyte hypertrophy in female rodents

doi: 10.1016/j.mce.2017.11.004

Figure Lengend Snippet: (a) TGFβ stimulates p38α activity, inhibited by SB2036580 or β-LGND. Bar graph is the mean±SD from 3 exps combined. *p < 0.05 vs. control, +p < 0.05 for TGFβ vs same + SB2036580 or β-LGND. (b) TGFβ inhibits KLF15 mRNA and protein in cardiomyocytes, blocked by the p38 antagonist SB2036580 (0.1μM) (c) TAK1 activating phosphorylation is stimulated by AngII or TGFβ, inhibited by β-LGND. *p<0.05 vs. control, + p<0.05 for TGFβ or AngII vs same plus β-LGND, n=3 exps. (d) TAK1 siRNA diminishes TGFβ or AngII-stimulated p38α activity. The latter was seen as phosphorylation at tyrosine182. *p<0.05 vs control, +p<0.05 for TGFβ or AngII vs same + β-LGND, n=3 exps. TAK1 siRNA validation is also shown. (e) Flow cytometry analysis of β-LGND inhibition of phospho-kinases due to cAMP/PKA. *p<0.05 for control vs. AngII-stimulated phospho-TAK1, phospho-p38α, or KLF15 proteins. +p<0.05 for AngII vs AngII + β-LGND, ++p<0.05 for AngII + β-LGND vs same + either H-89 (PKA inhibitor) or RP-8-Br-cAMP (cAMP inhibitor), n=3 exps.

Article Snippet: Additional antibodies and phospho-specific antibodies used for immuno-blots were obtained from the followings: Cell Signaling Technology (Danvers, MA) TAK1 (D94D7) (#5206), Phospho-ATF-2 (Thr71) (#9221), Phospho-TAK1 (Thr187) (#4536); Santa Cruz, Biotechnology (Dallas, TX), KLF15 (A5) (SC-271675), GAPDH (0411) (sc-47724), MYH7 (A4.951) (sc-53090), Actin (2Q1055) (sc-58673), p38 Antibody (A-20) (sc-535), phospho-p38 (Thr 180/Tyr 182) (sc-17852-R); (Boster Biological Technology, Pleasanton, CA), ACTA2 (M01072–1).

Techniques: Activity Assay, Control, Phospho-proteomics, Biomarker Discovery, Flow Cytometry, Inhibition

Journal: Molecular and cellular endocrinology

Article Title: Estrogen receptor beta maintains expression of KLF15 to prevent cardiac myocyte hypertrophy in female rodents

doi: 10.1016/j.mce.2017.11.004

Figure Lengend Snippet: AngII acting through TGFβ stimulates a TAK1-p38α kinase axis that inhibits KLF15 expression and nuclear localization of the protein. This contributes to increased gene expression and cardiomyocyte hypertrophy. ERβ acting through protein kinase A opposes TAK1-p38α activation. This restores KLF15 abundance and nuclear localization, contributing in part to inhibition of AngII-induced gene expression and cardiomyocyte hypertrophy.

Article Snippet: Additional antibodies and phospho-specific antibodies used for immuno-blots were obtained from the followings: Cell Signaling Technology (Danvers, MA) TAK1 (D94D7) (#5206), Phospho-ATF-2 (Thr71) (#9221), Phospho-TAK1 (Thr187) (#4536); Santa Cruz, Biotechnology (Dallas, TX), KLF15 (A5) (SC-271675), GAPDH (0411) (sc-47724), MYH7 (A4.951) (sc-53090), Actin (2Q1055) (sc-58673), p38 Antibody (A-20) (sc-535), phospho-p38 (Thr 180/Tyr 182) (sc-17852-R); (Boster Biological Technology, Pleasanton, CA), ACTA2 (M01072–1).

Techniques: Expressing, Gene Expression, Activation Assay, Inhibition

Journal: Frontiers in Immunology

Article Title: The diagnostic accuracy of CC chemokine ligand 23 for Kawasaki disease

doi: 10.3389/fimmu.2026.1758367

Figure Lengend Snippet: Intergroup comparison of CCL23 protein expression among the Kawasaki disease (KD) group, fever control (FC) group, and healthy control (HC) group.

Article Snippet: Meanwhile, the quantitative detection of CCL23 protein was conducted using the Human CCL23 ELISA Kit (Boster Biological Technology, Product No.: EK1224) in strict accordance with the kit instructions.

Techniques: Comparison, Expressing, Control

Journal: Frontiers in Immunology

Article Title: The diagnostic accuracy of CC chemokine ligand 23 for Kawasaki disease

doi: 10.3389/fimmu.2026.1758367

Figure Lengend Snippet: Diagnostic accuracy analysis of CC Chemokine Ligand 23 (CCL23) for Kawasaki disease (KD). (A) Comparison between the KD group and the fever control (FC) group; (B) Comparison between the KD group and the healthy control (HC) group; (C) Comparison between the KD group and the combined FC and HC groups.

Article Snippet: Meanwhile, the quantitative detection of CCL23 protein was conducted using the Human CCL23 ELISA Kit (Boster Biological Technology, Product No.: EK1224) in strict accordance with the kit instructions.

Techniques: Diagnostic Assay, Comparison, Control

Journal: Nature Communications

Article Title: IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3

doi: 10.1038/s41467-025-67456-3

Figure Lengend Snippet: a ChIP analysis of H3K27me3 or IgG at indicated promoters in keratinocytes with (white) or without (blue) IL-17A stimulation. Itga3: n = 5 (unstimulated), n = 4 (IL-17A-stimulated) technical replicates, p = 0.0034, Timp1 : n = 3 technical replicates, p = 0.0046, Ccl20 : n = 3 technical replicates, p = 0.0059, Cxcl1 : n = 3 technical replicates, p = 0.0020, Cxcl3 : n = 3 technical replicates, p = 0.0258, Cxcl5 : n = 3 technical replicates, p = 0.0174. n = 3 independent experiments. b qPCR analysis of keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (1 µM) (red). Itga3 : n = 4 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0017 (IL-17A vs. IL-17A and inhibitor), Timp1: n = 6 biological replicates, p < 0.0312 (DMSO vs. IL-17A), p = 0.0029 (IL-17A vs. IL-17A and inhibitor), Ccl20: n = 3 biological replicates, p = 0.0008 (DMSO vs. IL-17A), p = 0.0428 (IL-17A vs. IL-17A and inhibitor), Cxcl1 : n = 3 biological replicates, p = 0.0003 (DMSO vs. IL-17A), p = 0.0294 (IL-17A vs. IL-17A and inhibitor), Cxcl3 : n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0003 (IL-17A vs. IL-17A and inhibitor), Cxcl5 : n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0007 (IL-17A vs. IL-17A and inhibitor), n = 3 independent experiments. c Western blot of ITGA-3 expression in keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (red). Representative densitometry plot is shown. n = 3 independent experiments. d Protein quantification of lysates from keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (red). TIMP-1: n = 6 biological replicates, p = 0.0012 (DMSO vs. IL-17A), p = 0.0068 (IL-17A vs. IL-17A and inhibitor), CCL-20: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0199 (IL-17A vs. IL-17A and inhibitor), CXCL-1: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0158 (IL-17A vs. IL-17A and inhibitor), CXCL-3: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0167 (IL-17A vs. IL-17A and inhibitor), CXCL-5: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0005 (IL-17A vs. IL-17A and inhibitor), n = 3 independent experiments. e qPCR analysis of keratinocytes treated with a non-targeting control (siNTC) (white) or si Jmjd3 (gray). Jmjd3 : n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0192, Itga3: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0019, Timp1: n = 3 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0205, Ccl20: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0015, Cxcl1: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0019, Cxcl3: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0011, Cxcl5: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0011, n = 3 independent experiments. f qPCR analysis of Jmjd3 fl/fl K14 cre+ (red) and Jmjd3 fl/fl K14 cre- (yellow) keratinocytes. n = 3 biological replicates, Itga3 : p = 0.0184, Timp1 : p = 0.0044, Ccl20 : p = 0.0160, Cxcl1 : p = 0.0371, Cxcl3 : p = 0.0042. n = 3 independent experiments. g , h Scratch assays of primary murine ( n = 3 biological replicates, p < 0.0001 (48 h)) and N/TERT ( n = 3 biological replicates, p = 0.0340 (12 h)) keratinocytes treated with IL-17A alone (blue) or IL-17A and GSK-J4 (red). n = 3 independent experiments. i , j Scratch assays of primary murine ( n = 3 biological replicates, p = 0.0016 (48 h)) and N/TERT ( n = 6 biological replicates (IL-17A alone), n = 4 biological replicates (IL-17A and GSK-J1), p = 0.0223 (8 h), p < 0.0001 (12 h)) keratinocytes treated with IL-17A alone (blue) or IL-17A and GSK-J1 (red). n = 3 independent experiments. k Scratch assay of Jmjd3 fl/fl K14 cre+ (red) and Jmjd3 fl/fl K14 cre- (blue) keratinocytes. n = 3 biological replicates, p = 0.0198 (48 h). n = 3 independent experiments. Data were analyzed for variances, and 2-tailed Student’s t tests for ( a ), ( e ), ( f ) and 1-way ANOVA tests for ( b ), ( d ), ( g – k ) were performed. Data are presented as the mean ± SEM.

Article Snippet: After stimulation, cell free supernatant was collected and analyzed by the University of Michigan Immune Monitoring Shared Resource Core for CCL-20, CXCL-1, CXCL-5 or specific enzyme immunoassay kits for CXCL-3 (Boster Bio) and TIMP-1 (R&D Systems) according to the manufacturer’s instructions.

Techniques: Western Blot, Expressing, Control, Wound Healing Assay

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 4. Validation of differentially expressed mRNAs, lncRNAs, and miRNAs (n ¼ 3). Notes: (A) mRNA expression levels of Ccl4, Clec4e, CXCL2, Acod1, Bcl2a1d, Ccl3, Dusp2, Dusp5, Glrx, IL27, Itga5, Nfkbia, Nfkbid, Nfkbiz, Nlrp3, Pdgfb, Tnf and Tnfrsf1b. (B) lncRNA expression levels of ENSMUST00000174829, ENSMUST0000034789, ENSMUST0000074287, ENSMUST0000022589, MSTRG.12908.1 and MSTRG.5823.1. (C) miRNA expression levels of miR-21-z, miR-17-x, miR-212-x, miR-217-x, and miR-342-y.

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Biomarker Discovery, Expressing

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 5. CXCL2-miR-217-X-MSTRG.5823.1 network construction. Notes: (A) Co differentially expressed mRNA, miRNA and lncRNA in the ctrl vs PCV2 com- parison group and PCV2 vs PCV2 + SSP comparison group shown by Venn diagram. (B) KEGG pathway analysis of 78 differentially co-expressed mRNAs (C) GO pathway analysis of 78 differentially co-expressed mRNAs. (D) Subcellular localization of lncRNA MSTRG.5823.1, with MSTRG.5823.1 probe in red and DAPI nuclear staining in blue, and no overlap between red and blue, indicating that MSTRG.5823.1 is located in the cytoplasm. (E) Prediction of targeting relationship between MSTRG.5823.1-miR-217-x- CXCL2. (F) In the ceRNA network, red represents up-regulation, green represents down-regulation, circles represent mRNA, triangles represent miRNAs, diamonds represent lncRNAs, and the solid line indicates the targeting relationship. (G) Targeted binding relationship between CXCL2 and miR- 217-x (n = 3). (H) Target binding relationship between MSTRG.5823.1 and miR-217-x (n = 3). Error bars are represented as means ± SD. *p value < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Comparison, Staining, Binding Assay

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 6. Effect of miR-217-x in PCV2-infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of overexpression miR-217-x on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in PCV2 infected RAW264.7 cells. (B) Effect of overexpression miR-217-x on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in PCV2 infection group. (C-E) Effects of overexpression miR-217-x on the expression levels of CXCl2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 proteins in PCV2 infected RAW264.7 cells. (F) Effect of knockdown miR-217-x on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α. (G) Effect of knockdown miR-217-x on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in PCV2 infected RAW264.7 cells. (H-J) Effect of knockdown miR-217-x on the expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 proteins in PCV2 infected RAW264.7 cells. Error bars are represented as means ± SD. Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 7. The function of miR-217-x in SSP-treated PCV2-infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of overexpression miR-217-x on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in SSP treatment group. (B) Effect of overexpression miR-217-x on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in SSP-treated −RAW264.7 cells infected with PCV2. (C-E) Effect of overexpression miR-217-x on the expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p- IKKβ, p65and p-p65 proteins in SSP treatment group. (F) Effect of knockdown miR-217-x on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in SSP-treated RAW264.7 cells infected with PCV2. (G) Effect of knockdown miR-217-x on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in SSP treatment group. (H-J) Effect of knockdown miR-217-x on the protein expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65and p-p65 in SSP treatment group. Error bars are represented as means ± SD Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 8. The function of lncRNA-MSTRG.5823.1 in PCV2-infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of overexpression of MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in PCV2-infected RAW264.7 cells. (B) Effect of overexpression of MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in PCV2-infected RAW264.7 cells. (C-E) Effect of overexpression of MSTRG.5823.1 on the protein expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65and p-p65 in PCV2-infected RAW264.7 cells. (F) Effect of knockdown MSTRG.5823.1 on the expression levels of miR- 217-x, MSTRG.5823.1, Rel and TNF-α. (G) Effect of knockdown MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in PCV2-infected RAW264.7 cells. (H-J) Effect of knockdown MSTRG.5823.1 on the protein expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 in PCV2- infected RAW264.7 cells. Error bars are represented as means ± SD. Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 9. The function of lncRNA-MSTRG.5823.1 in SSP-treated PCV2-infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of overexpression of MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel, TNF-α in SSP treatment group. (B) Effect of overexpression of MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in SSP treatment group. (C-E) Effect of overexpression of MSTRG.5823.1 on the protein expression levels of CXCL2, TNF-α, IKB, p- IKB, IKKβ, p-IKKβ, p65 and p-p65 in SSP treatment group. (F) Effect of knockdown MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in SSP treatment group. (G) Effect of knockdown MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, IL-1β mRNA in SSP treatment group. (H-J) Effect of knockdown MSTRG.5823.1 on the expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 proteins in SSP treatment group. Error bars are represented as means ± SD. Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), and shoulder labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 10. Effect of the MSTRG.5823.1/miR-217-x/CXCL2 axis on immunosuppression in PCV2-infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of over- expression of miR-217-x and MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in PCV2 infection group. (B) Effect of over- expression of miR-217-x and MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in in PCV2 infection group. (C-E) Effect of overexpression of miR-217-x and MSTRG.5823.1 on CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 protein expression levels in in PCV2 infection group. (F) Effect of knockdown miR-217-x and MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α. (G) Effect of knockdown miR-217-x and MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in PCV2-infected RAW264.7 cells. (H-J) Effect of knockdown miR-217-x and MSTRG.5823.1 on the protein expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 in PCV2-infected RAW264.7 cells. Error bars are rep- resented as means ± SD. Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 11. SSP promoted activation of the TNF/NF-κB pathway by regulating MSTRG.5823.1/miR-217-x/CXCL2 axis in PCV2- infected RAW264.7 cells (n ¼ 3). Notes: (A) Effect of overexpression of miR-217-x and MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1, Rel and TNF-α in SSP treatment group. (B) Effect of overexpression of miR-217-x and MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in SSP treatment group. (C-E) Effect of overexpression of miR-217-x and MSTRG.5823.1 on the expression levels of CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65and p-p65 proteins in SSP treatment group. (F) Effect of knockdown miR-217-x and MSTRG.5823.1 on the expression levels of miR-217-x, MSTRG.5823.1 and Rel, TNF-α in SSP treatment group. (G) Effect of knockdown miR-217-x and MSTRG.5823.1 on the expression levels of CXCL2, CXCL10, and IL-1β mRNA in SSP treatment group. (H-J) Effect of knockdown miR-217-x and MSTRG.5823.1 on CXCL2, TNF-α, IKB, p-IKB, IKKβ, p-IKKβ, p65 and p-p65 protein expression levels in SSP treatment group. Error bars are represented as means ± SD. Shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: Activation Assay, Infection, Over Expression, Expressing, Knockdown

Journal: International immunopharmacology

Article Title: Sophora subprostrate polysaccharide targets LncRNA MSTRG.5823.1 to suppress PCV2-mediated immunosuppression via TNF/NF-κB signaling.

doi: 10.1016/j.intimp.2024.112701

Figure Lengend Snippet: Fig. 12. Effects of SSP on the regulation of PCV2-induced immunosuppression model in mice (n ¼ 12). Notes: (A) Schematic representation of PCV2-induced immunosuppression in vivo model: BALB/c mice were injected intraperitoneally with PCV2 (TCID50 = 10-5/0.1 mL) on the first day of the experiment, and SSP (200 mg/kg•BW) was administered by gavage every day for 7 days. (B-E) secretion levels of CXCL2, CXCL10, TNF-α and IL-1β in thymus tissue homogenate. (F) His- topathological examination of lungs, spleens, livers, and thymus of all three animal groups. [control group, PCV2-infected group, PCV2 + SSP (200 mg/kg•BW)]. scale Bar: 100 µm. (Gray boxes indicate the site of PCV2-induced lesions in tissues. scale Bar: 20 µm.) (G-J) Protein expression levels of TNF-α and CXCL2 in lungs, spleens, livers, and thymuses of all three groups of animals [control group, PCV2-infected group, PCV2 + SSP (200 mg/kg•BW)]. scale Bar: 100 µm. (K) Expression levels of p65 and p-p65 in the thymus from all three animal groups[control group, PCV2-infected group, PCV2 + SSP (200 mg/kg•BW)]. scale Bar: 50 µm. Error bars are represented as means ± SE shoulder labels with the same alphabet indicate non-significant differences (p > 0.05), while labels with different alphabets indicate significant differences (p < 0.05).

Article Snippet: The primary antibody against rabbit CXCL2 (pb0900, 1:500 dilution) was obtained from BOSTER (California, USA).

Techniques: In Vivo, Injection, Control, Infection, Expressing

Journal: Naunyn-Schmiedeberg's Archives of Pharmacology

Article Title: The effects of melatonin on oxidative stress, inflammation, apoptosis and Nrf2/HO-1 in acrylamide-induced lung injury in rats

doi: 10.1007/s00210-025-04292-8

Figure Lengend Snippet: Lung TNF-α, IL-1β, IL-6, NF-κB, iNOS, COX-2, MPO, p38 MAPK, and IL-10 activities in experimental groups ( n = 10). Results are expressed as mean ± SEM

Article Snippet: Catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), heme oxygenase 1 (HO-1), interleukin-1 beta (IL-1β), interleukin-10 (IL-10), malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear factor kappa (NF-κB), superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α), caspase 3 (CASP3), inducible nitric oxide synthase (iNOS; NOS2), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), p38 mitogen-activated protein kinases (p38-MAPK), and myeloperoxidase (MPO) enzyme-linked immunosorbent assay (ELISA) kits were purchased from BT-LAB.

Techniques: