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The effect of berberine on circulating anti-bovine type II collagen <t>(CII)</t> <t>IgG</t> in the CIA model. ( A ) Anti-CII IgG1, IgG2a, and total IgG at day 28 among all mice (arthritic and non-arthritic) within BBR, PBS (vehicle control), CIA (no treatment control), and non-CIA control animals ( n = 10 per group). ( B ) Anti-CII IgG levels at day 28 compared among arthritic mice only (BBR n = 5; PBS n = 9; CIA n = 9). Statistical comparisons made with the Kruskal–Wallis test with Dunn’s multiple comparisons. ( C ) Anti-CII IgG levels at day 28 compared among BBR-treated mice who developed arthritis (“arthritic”) vs. those that did not (“non-arthritic”). Statistical comparisons made with the Mann–Whitney U test. For all statistical tests in A–C, * p < 0.05, ** p < 0.01, **** p < 0.0001.
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PRDX1-OE attenuates the disease progression of RA by inhibiting plasma cell differentiation. (A) The clinical arthritis severity score was assessed in WT and Prdx1 -OE mice immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative images of paws from the WT and PRDX1-OE group. (C) Representative micro-CT images of paws from the WT and PRDX1-OE groups. (D) Joint destruction from the WT and PRDX1-OE groups was graded using CT score ( n = 3). (E) Representative images of H&E-stained sections of ankle joints from the WT and PRDX1-OE groups are shown. Scale bar, 500 μm. (F) Histopathology analysis and histological scoring were performed on ankle joints from the WT and PRDX1-OE groups ( n = 6). (G) Serum levels of <t>IgG2A</t> were analyzed by ELISA in WT and PRDX1-OE model groups ( n = 6). (H) The proportion of plasma cells in the spleen was analyzed by flow cytometry. (I) A quantitative analysis of plasma cell counts in the spleens of Prdx1 -OE and wild-type mice ( n = 6). (J) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the spleens of Prdx1 -OE and WT model mice. Data are shown as mean ± SEM, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
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PRDX1-OE attenuates the disease progression of RA by inhibiting plasma cell differentiation. (A) The clinical arthritis severity score was assessed in WT and Prdx1 -OE mice immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative images of paws from the WT and PRDX1-OE group. (C) Representative micro-CT images of paws from the WT and PRDX1-OE groups. (D) Joint destruction from the WT and PRDX1-OE groups was graded using CT score ( n = 3). (E) Representative images of H&E-stained sections of ankle joints from the WT and PRDX1-OE groups are shown. Scale bar, 500 μm. (F) Histopathology analysis and histological scoring were performed on ankle joints from the WT and PRDX1-OE groups ( n = 6). (G) Serum levels of <t>IgG2A</t> were analyzed by ELISA in WT and PRDX1-OE model groups ( n = 6). (H) The proportion of plasma cells in the spleen was analyzed by flow cytometry. (I) A quantitative analysis of plasma cell counts in the spleens of Prdx1 -OE and wild-type mice ( n = 6). (J) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the spleens of Prdx1 -OE and WT model mice. Data are shown as mean ± SEM, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
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PRDX1-OE attenuates the disease progression of RA by inhibiting plasma cell differentiation. (A) The clinical arthritis severity score was assessed in WT and Prdx1 -OE mice immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative images of paws from the WT and PRDX1-OE group. (C) Representative micro-CT images of paws from the WT and PRDX1-OE groups. (D) Joint destruction from the WT and PRDX1-OE groups was graded using CT score ( n = 3). (E) Representative images of H&E-stained sections of ankle joints from the WT and PRDX1-OE groups are shown. Scale bar, 500 μm. (F) Histopathology analysis and histological scoring were performed on ankle joints from the WT and PRDX1-OE groups ( n = 6). (G) Serum levels of <t>IgG2A</t> were analyzed by ELISA in WT and PRDX1-OE model groups ( n = 6). (H) The proportion of plasma cells in the spleen was analyzed by flow cytometry. (I) A quantitative analysis of plasma cell counts in the spleens of Prdx1 -OE and wild-type mice ( n = 6). (J) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the spleens of Prdx1 -OE and WT model mice. Data are shown as mean ± SEM, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
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PLD1 deficiency suppresses <t>the</t> <t>collagen</t> type II-specific humoral response and the production of proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen total <t>IgG,</t> IgG1, and IgG2a antibodies was measured by ELISA in the serum from the indicated mice at day 42. ( B ) Measurement of proinflammatory cytokines in the serum of the indicated mice at day 42 as analyzed by ELISA. n = 15 per group. * p < 0.05, N.S., non-significant. Results are shown as mean ± standard error of the mean (SEM).
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PLD1 deficiency suppresses <t>the</t> <t>collagen</t> type II-specific humoral response and the production of proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen total <t>IgG,</t> IgG1, and IgG2a antibodies was measured by ELISA in the serum from the indicated mice at day 42. ( B ) Measurement of proinflammatory cytokines in the serum of the indicated mice at day 42 as analyzed by ELISA. n = 15 per group. * p < 0.05, N.S., non-significant. Results are shown as mean ± standard error of the mean (SEM).
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PLD1 deficiency suppresses <t>the</t> <t>collagen</t> type II-specific humoral response and the production of proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen total <t>IgG,</t> IgG1, and IgG2a antibodies was measured by ELISA in the serum from the indicated mice at day 42. ( B ) Measurement of proinflammatory cytokines in the serum of the indicated mice at day 42 as analyzed by ELISA. n = 15 per group. * p < 0.05, N.S., non-significant. Results are shown as mean ± standard error of the mean (SEM).
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Image Search Results


The effect of berberine on circulating anti-bovine type II collagen (CII) IgG in the CIA model. ( A ) Anti-CII IgG1, IgG2a, and total IgG at day 28 among all mice (arthritic and non-arthritic) within BBR, PBS (vehicle control), CIA (no treatment control), and non-CIA control animals ( n = 10 per group). ( B ) Anti-CII IgG levels at day 28 compared among arthritic mice only (BBR n = 5; PBS n = 9; CIA n = 9). Statistical comparisons made with the Kruskal–Wallis test with Dunn’s multiple comparisons. ( C ) Anti-CII IgG levels at day 28 compared among BBR-treated mice who developed arthritis (“arthritic”) vs. those that did not (“non-arthritic”). Statistical comparisons made with the Mann–Whitney U test. For all statistical tests in A–C, * p < 0.05, ** p < 0.01, **** p < 0.0001.

Journal: International Journal of Molecular Sciences

Article Title: Berberine Delays Onset of Collagen-Induced Arthritis through T Cell Suppression

doi: 10.3390/ijms22073522

Figure Lengend Snippet: The effect of berberine on circulating anti-bovine type II collagen (CII) IgG in the CIA model. ( A ) Anti-CII IgG1, IgG2a, and total IgG at day 28 among all mice (arthritic and non-arthritic) within BBR, PBS (vehicle control), CIA (no treatment control), and non-CIA control animals ( n = 10 per group). ( B ) Anti-CII IgG levels at day 28 compared among arthritic mice only (BBR n = 5; PBS n = 9; CIA n = 9). Statistical comparisons made with the Kruskal–Wallis test with Dunn’s multiple comparisons. ( C ) Anti-CII IgG levels at day 28 compared among BBR-treated mice who developed arthritis (“arthritic”) vs. those that did not (“non-arthritic”). Statistical comparisons made with the Mann–Whitney U test. For all statistical tests in A–C, * p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: Serum concentrations of anti-collagen type II (anti-CII) total IgG (catalog # 1012T), anti-CII IgG1 (catalog # 20321T), and anti-CII IgG2a (catalog # 20322T) were measured by ELISA (Chondrex, Redmond, WA, USA) according to the manufacturer’s instructions [ , ].

Techniques: MANN-WHITNEY

PRDX1-OE attenuates the disease progression of RA by inhibiting plasma cell differentiation. (A) The clinical arthritis severity score was assessed in WT and Prdx1 -OE mice immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative images of paws from the WT and PRDX1-OE group. (C) Representative micro-CT images of paws from the WT and PRDX1-OE groups. (D) Joint destruction from the WT and PRDX1-OE groups was graded using CT score ( n = 3). (E) Representative images of H&E-stained sections of ankle joints from the WT and PRDX1-OE groups are shown. Scale bar, 500 μm. (F) Histopathology analysis and histological scoring were performed on ankle joints from the WT and PRDX1-OE groups ( n = 6). (G) Serum levels of IgG2A were analyzed by ELISA in WT and PRDX1-OE model groups ( n = 6). (H) The proportion of plasma cells in the spleen was analyzed by flow cytometry. (I) A quantitative analysis of plasma cell counts in the spleens of Prdx1 -OE and wild-type mice ( n = 6). (J) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the spleens of Prdx1 -OE and WT model mice. Data are shown as mean ± SEM, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Augmentation of PRDX1–DOK3 interaction alleviates rheumatoid arthritis progression by suppressing plasma cell differentiation

doi: 10.1016/j.apsb.2025.06.006

Figure Lengend Snippet: PRDX1-OE attenuates the disease progression of RA by inhibiting plasma cell differentiation. (A) The clinical arthritis severity score was assessed in WT and Prdx1 -OE mice immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative images of paws from the WT and PRDX1-OE group. (C) Representative micro-CT images of paws from the WT and PRDX1-OE groups. (D) Joint destruction from the WT and PRDX1-OE groups was graded using CT score ( n = 3). (E) Representative images of H&E-stained sections of ankle joints from the WT and PRDX1-OE groups are shown. Scale bar, 500 μm. (F) Histopathology analysis and histological scoring were performed on ankle joints from the WT and PRDX1-OE groups ( n = 6). (G) Serum levels of IgG2A were analyzed by ELISA in WT and PRDX1-OE model groups ( n = 6). (H) The proportion of plasma cells in the spleen was analyzed by flow cytometry. (I) A quantitative analysis of plasma cell counts in the spleens of Prdx1 -OE and wild-type mice ( n = 6). (J) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the spleens of Prdx1 -OE and WT model mice. Data are shown as mean ± SEM, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

Article Snippet: The serum was subjected to calculate the concentrations of IgG2A using the Mouse anti-bovine type II collagen IgG2A antibody subtype ELISA kit with TMB (Chondrex, 20322T).

Techniques: Biomarker Discovery, Clinical Proteomics, Cell Differentiation, Adjuvant, Micro-CT, Staining, Histopathology, Enzyme-linked Immunosorbent Assay, Flow Cytometry

Salvianolic acid B prevents the progression of collagen-induced arthritis by enhancing the interaction between PRDX1 and DOK3. (A) Clinical scores of arthritis in mice treated with vehicle, 1.5 mg/kg TF, and 15 mg/kg or 30 mg/kg SAB, and immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative micro-CT images of the hind paws from mice treated with vehicle, TF, and SAB. (C) Joint destruction was graded based on the CT score in B ( n = 3). (D, E) histological score of the inflammation area in mice treated with vehicle, TF, and SAB ( n = 6) (D) and representative images of hematoxylin and eosin (H&E)-stained paw sections (E). Scale bar, 100 μm. (F) Serum titer of IgG2A analyzed from vehicle, TF, and SAB by ELISA ( n = 6). (G, H) The frequency of plasma cells (G) and GC B cells (H) in the spleen from mice treated with vehicle, TF, and SAB was analyzed by flow cytometry ( n = 6). (I) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the SAB-H treatment and model groups. (J) Heatmap depicting the expression levels of the B cell receptor signaling pathway and RA defined by the differentially downregulated genes in the SAB-H treatment group compared to the WT model group. (K) The biological process analysis of B cells for downregulated genes in the SAB-H treatment group compared to the model group. (L) Representative immunofluorescence staining images of PRDX1 (green) and DOK3 (red) in the spleen from the model and SAB treatment groups. Scale bar, 50 μm. (M) Representative immunofluorescence staining images of CD19 (green), P-JNK (red) in the spleen from the model and SAB treatment groups. Scale bar, 50 μm. (N) Relative fluorescence intensity of stained PRDX1 and DOK3 in the spleen from the model and SAB treatment groups ( n = 3). (O) Relative fluorescence intensity of stained CD19 and P-JNK in the spleen from the model and SAB treatment groups ( n = 3). Data are presented as mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, and ns indicates no significance.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Augmentation of PRDX1–DOK3 interaction alleviates rheumatoid arthritis progression by suppressing plasma cell differentiation

doi: 10.1016/j.apsb.2025.06.006

Figure Lengend Snippet: Salvianolic acid B prevents the progression of collagen-induced arthritis by enhancing the interaction between PRDX1 and DOK3. (A) Clinical scores of arthritis in mice treated with vehicle, 1.5 mg/kg TF, and 15 mg/kg or 30 mg/kg SAB, and immunized with collagen in complete Freund's adjuvant ( n = 6). (B) Representative micro-CT images of the hind paws from mice treated with vehicle, TF, and SAB. (C) Joint destruction was graded based on the CT score in B ( n = 3). (D, E) histological score of the inflammation area in mice treated with vehicle, TF, and SAB ( n = 6) (D) and representative images of hematoxylin and eosin (H&E)-stained paw sections (E). Scale bar, 100 μm. (F) Serum titer of IgG2A analyzed from vehicle, TF, and SAB by ELISA ( n = 6). (G, H) The frequency of plasma cells (G) and GC B cells (H) in the spleen from mice treated with vehicle, TF, and SAB was analyzed by flow cytometry ( n = 6). (I) GSEA enrichment profiles of the B cell receptor pathway and CD40 pathway in the SAB-H treatment and model groups. (J) Heatmap depicting the expression levels of the B cell receptor signaling pathway and RA defined by the differentially downregulated genes in the SAB-H treatment group compared to the WT model group. (K) The biological process analysis of B cells for downregulated genes in the SAB-H treatment group compared to the model group. (L) Representative immunofluorescence staining images of PRDX1 (green) and DOK3 (red) in the spleen from the model and SAB treatment groups. Scale bar, 50 μm. (M) Representative immunofluorescence staining images of CD19 (green), P-JNK (red) in the spleen from the model and SAB treatment groups. Scale bar, 50 μm. (N) Relative fluorescence intensity of stained PRDX1 and DOK3 in the spleen from the model and SAB treatment groups ( n = 3). (O) Relative fluorescence intensity of stained CD19 and P-JNK in the spleen from the model and SAB treatment groups ( n = 3). Data are presented as mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, and ns indicates no significance.

Article Snippet: The serum was subjected to calculate the concentrations of IgG2A using the Mouse anti-bovine type II collagen IgG2A antibody subtype ELISA kit with TMB (Chondrex, 20322T).

Techniques: Adjuvant, Micro-CT, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Flow Cytometry, Expressing, Immunofluorescence, Fluorescence

PLD1 deficiency suppresses the collagen type II-specific humoral response and the production of proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen total IgG, IgG1, and IgG2a antibodies was measured by ELISA in the serum from the indicated mice at day 42. ( B ) Measurement of proinflammatory cytokines in the serum of the indicated mice at day 42 as analyzed by ELISA. n = 15 per group. * p < 0.05, N.S., non-significant. Results are shown as mean ± standard error of the mean (SEM).

Journal: International Journal of Molecular Sciences

Article Title: Targeting of Phospholipase D1 Ameliorates Collagen-Induced Arthritis via Modulation of Treg and Th17 Cell Imbalance and Suppression of Osteoclastogenesis

doi: 10.3390/ijms21093230

Figure Lengend Snippet: PLD1 deficiency suppresses the collagen type II-specific humoral response and the production of proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen total IgG, IgG1, and IgG2a antibodies was measured by ELISA in the serum from the indicated mice at day 42. ( B ) Measurement of proinflammatory cytokines in the serum of the indicated mice at day 42 as analyzed by ELISA. n = 15 per group. * p < 0.05, N.S., non-significant. Results are shown as mean ± standard error of the mean (SEM).

Article Snippet: The amount of murine CII-specific autoantibodies in the serum was measured using the Mouse Anti-Type II Collagen IgG Subtype Antibody Assay Kit (Chondrex), according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay

The PLD1 inhibitor reduces the production of the anti-CII IgG2a autoantibody and proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen IgG1 and IgG2a antibodies was measured by ELISA in the serum of the indicated mice at day 45. ( B ) The amount of proinflammatory cytokines was measured by ELISA in the serum of the indicated mice at day 45. n = 15 per group. * p < 0.05. Results are shown as mean ± standard error of the mean (SEM).

Journal: International Journal of Molecular Sciences

Article Title: Targeting of Phospholipase D1 Ameliorates Collagen-Induced Arthritis via Modulation of Treg and Th17 Cell Imbalance and Suppression of Osteoclastogenesis

doi: 10.3390/ijms21093230

Figure Lengend Snippet: The PLD1 inhibitor reduces the production of the anti-CII IgG2a autoantibody and proinflammatory cytokines in collagen-induced arthritis (CIA) mice. ( A ) The amount of anti-collagen IgG1 and IgG2a antibodies was measured by ELISA in the serum of the indicated mice at day 45. ( B ) The amount of proinflammatory cytokines was measured by ELISA in the serum of the indicated mice at day 45. n = 15 per group. * p < 0.05. Results are shown as mean ± standard error of the mean (SEM).

Article Snippet: The amount of murine CII-specific autoantibodies in the serum was measured using the Mouse Anti-Type II Collagen IgG Subtype Antibody Assay Kit (Chondrex), according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay