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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 <t>IL‐1α,</t> <t>IL‐6,</t> <t>IL‐17A</t> and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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In vivo validation of key targets. (A) Expression levels of IL-1β, <t>IL-17A,</t> 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.
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Image Search Results


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.

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

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.

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

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.

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

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.

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

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.

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

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.

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