Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Topical calcitriol application ameliorates IMQ‐induced psoriasis in mice. (A) Schematic illustration of the unilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the right ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of right ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Staining, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Topical calcitriol treatment ameliorates distant psoriatic skin lesions in the bilateral ear model. (A) Schematic illustration of the bilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the left ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of left ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. ** p < 0.01, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Staining, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Calcitriol ameliorates M5‐induced abnormal proliferation, migration and inflammatory responses in HaCaT cells. (A) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (B) Cell viability was assessed in different treatment groups. (C) Colony formation assay was performed to evaluate the proliferative capacity of cells in each group. (D) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (E) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

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

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Calcitriol ameliorates M5‐induced psoriasis‐like phenotypes through CHI3L2 downregulation. (A) The mRNA expression of RPL36A, PPBP, UBE2F, MGC32805, IL4I1, LINC00519, CHI3L2, ABHD14A and PCDHGB7 , validated by RT‐qPCR assay. (B) Efficacy of shRNA‐mediated CHI3L2 knockdown confirmed by RT‐qPCR. (C) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (D) Cell viability was assessed in different treatment groups. (E) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (F) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Expressing, Quantitative RT-PCR, shRNA, Knockdown, Western Blot, Control, Wound Healing Assay

Journal: RSC Advances

Article Title: Exploring the anti-inflammatory targets of Gui-qi-yi-shen granules in diabetic nephropathy: insights from network pharmacology, transcriptomics, and experimental verification

doi: 10.1039/d6ra03780a

Figure Lengend Snippet: In vivo validation of key targets. (A) Expression levels of IL-1β, IL-17A, and CDKN1A were detected by RT-PCR. (B) Expression levels of IL-1β, p21, and activated JUN were detected by western blot. (C) Densitometric analysis of the bands in Fig. 9B was performed. The relative expression levels of IL-1β and p21 were normalized to β-actin, while pJUN/JUN is presented as the ratio of phosphorylated to total protein. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The membranes were incubated with primary antibodies against IL-1β (proteintech, 26048-1-AP), JUN (proteintech, 24909-1-AP), P-JUN (proteintech, 80086-1-RR), P21 (proteintech, 10355-1-AP), IL-17A (Abclonal, A12454) and β-actin (proteintech, 66009-1-Ig), followed by IRDye 800CW Goat anti-mouse IgG (H + L) or IRDye 680RD Goat anti-Rabbit IgG (H + L).

Techniques: In Vivo, Biomarker Discovery, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot

Journal: RSC Advances

Article Title: Exploring the anti-inflammatory targets of Gui-qi-yi-shen granules in diabetic nephropathy: insights from network pharmacology, transcriptomics, and experimental verification

doi: 10.1039/d6ra03780a

Figure Lengend Snippet: Experimental validation was performed using immunofluorescence. (A) Immunostaining of IL-17A in each group. (B) The fluorescence intensity of IL-17A. (C) Immunostaining of pNF-κB in each group. (D) The fluorescence intensity of pNF-κB. Nuclei were stained with DAPI. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The membranes were incubated with primary antibodies against IL-1β (proteintech, 26048-1-AP), JUN (proteintech, 24909-1-AP), P-JUN (proteintech, 80086-1-RR), P21 (proteintech, 10355-1-AP), IL-17A (Abclonal, A12454) and β-actin (proteintech, 66009-1-Ig), followed by IRDye 800CW Goat anti-mouse IgG (H + L) or IRDye 680RD Goat anti-Rabbit IgG (H + L).

Techniques: Biomarker Discovery, Immunofluorescence, Immunostaining, Fluorescence, Staining

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes associated with the IL-17 signaling pathway in ischemic stroke. (A) Venn diagram showing the overlap between differentially expressed genes (DEGs) identified from GEO datasets and genes retrieved from the CellAge database. Five overlapping genes were identified: PTGS2, MMP9, SERPINB2, CTNNAL1, and HTRA1. CS, genes from CellAge database; DEG, significantly differentially expressed genes in ischemic stroke. (B) Gene Ontology (GO) enrichment analysis of the overlapping genes, including biological process, cellular component, and molecular function categories. (C) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showing that the overlapping genes were enriched in inflammation-related pathways, including the IL-17 signaling pathway and TNF signaling pathway. (D) GSEA comparing ischemic stroke (IS) and control samples, demonstrating enrichment of immune- and inflammation-related pathways in IS. (E) Predicted transcription factor–target gene regulatory network for PTGS2 and MMP9, showing candidate shared upstream transcription factors. Yellow nodes represent TFs, red nodes represent target genes.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Serum IL-17A, PTGS2, and MMP9 levels in the clinical cohort and their correlations with each other and with stroke severity. (A–C) Serum IL-17A, PTGS2, and MMP9 levels were significantly higher in patients with ischemic stroke than in healthy controls. IS, ischemic stroke (n = 104); Normal, control group (n = 58). (D) Correlations among serum IL-17A, PTGS2, and MMP9 levels in the stroke group. (E) Positive correlations between serum IL-17A, PTGS2, and MMP9 levels and admission NIHSS scores in patients with ischemic stroke. Correlations were analyzed using Spearman’s rank correlation test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: MCAO-induced activation of IL-17A/PTGS2/MMP9-related inflammatory markers and changes after anti-IL-17A antibody treatment in rat brain tissue. (A–C) Relative mRNA levels of PTGS2, MMP9, and IL-17A in the sham, MCAO, and anti-IL-17A Ab groups. (D–F) Protein concentrations of PTGS2, MMP9, and IL-17A. (G, H) Concentrations of PGE2 and IL-6. (I) Neurological deficit scores assessed using the Longa scoring system. In panel I, the sham group median was 0; therefore, a minimal bar height was displayed for visualization only. (J) Representative TTC-stained brain sections from the MCAO and anti-IL-17A Ab groups. White areas indicate infarct regions, whereas red areas indicate viable brain tissue. (K) Quantitative analysis of infarct volume percentage based on TTC staining. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Data in panels A-H are presented as mean ± SEM (n = 6 per group). Neurological deficit scores in panel I are presented as median (interquartile range) (n = 6 per group). TTC analysis in panels (J, K) was performed in an independent cohort of rats, with final sample sizes of n = 4 for the MCAO group and n = 5 for the anti-IL-17A Ab group; one rat in the MCAO group died before tissue collection. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Activation Assay, Staining

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Spearman correlation analyses among IL-17A, PTGS2, MMP9, PGE2, and IL-6 in rat brain tissue. Correlation analyses were performed using pooled data from all animals (n = 18). (A) Correlation between IL-17A and PTGS2 mRNA expression. (B) Correlation between IL-17A and MMP9 mRNA expression. (C) Correlation between IL-17A and PTGS2 protein expression. (D) Correlation between IL-17A and MMP9 protein expression. (E) Correlation between IL-17A and PGE2 levels. (F) Correlation between IL-17A and IL-6 levels. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Given the limited sample size, these correlations should be interpreted with caution.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Expressing