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Proteintech pdgfr β
Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Cell Signaling Technology Inc antibodies against (tlr4, nfκ-b, iκbα, il-6, tnf-α, tgf-β1, vegf-a, and pdgfr-β)
Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the <t>PDGF/PDGFR-β</t> signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.
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Image Search Results


Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the PDGF/PDGFR-β signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.

Journal: Pharmaceuticals

Article Title: Eupatorium lindleyanum DC Ameliorates Carbon Tetrachloride-Induced Hepatic Inflammation and Fibrotic Response in Mice

doi: 10.3390/ph18081228

Figure Lengend Snippet: Eup exerts anti-fibrotic effects by attenuating CCl 4 -induced liver fibrosis through modulation of the PDGF/PDGFR-β signaling pathway. ( A ) GSEA analyses of PDGF/PDGFR-β signaling pathway between the NC group and the 40 g/kg Eup group (n = 3 per group). ( B ) Representative immunoblot images demonstrating protein expression of GAPDH and PDGF-BB/PDGFR-β signaling pathway-related proteins. ( C – E ) The activation status of the PDGF-BB/PDGFR-β signaling pathway-related proteins was quantified through densitometric analysis using Image J (p-PDGFR-β/PDGFR-β, p-AKT/AKT, and p-ERK/ERK). GAPDH was the loading control. Data are presented as mean ± SD, n = 3. # p < 0.05 and ### p < 0.001 versus control group; * p < 0.05 and *** p < 0.001 versus CCl 4 group.

Article Snippet: For Western blot analysis, primary antibodies against β-actin (1:2500, abs171598, Absin, Shanghai, China), α-SMA (1:2500, Proteintech Group, Wuhan, China), Collagen I (1:2000, Proteintech Group, Wuhan, China), PDGFR-β (1:1250, Proteintech Group, Wuhan, China), p-PDGFR-β (1:1000, Abcam, UK), GAPDH (1:1500, Servicebio, Wuhan, China), p-AKT (1:1000, Abcam, UK), AKT (1:1000, Abcam, UK), p-ERK (1:1500, Selleck Chemicals, Houston, TX, USA) and ERK (1:1000, Selleck Chemicals, Houston, TX, USA), were applied.

Techniques: Western Blot, Expressing, Activation Assay, Control

Eup suppresses PDGF-BB-induced HSC activation by inhibiting the PDGF-BB/PDGFR-β signaling pathway. ( A ) LX-2 cells were cultured with 20 ng/mL PDGF-BB, 1, 10, and 20 μg/mL Eup for 24 h. ( B – E ) qRT-PCR analysis of α-SMA , Col1 , Col3 , and LOX in LX-2 cells administrated with different concentrations of Eup. ( F ) Representative immunoblot images demonstrating protein expression of GAPDH, α-SMA, p-PDGFR-β, PDGFR-β, p-AKT, AKT, p-ERK, and ERK. ( G – J ) Expression levels of α-SMA and phosphorylation ratios of PDGFR-β (p-PDGFR-β/PDGFR-β), AKT (p-AKT/AKT), and ERK (p-ERK/ERK). The loading control was GAPDH. Data are presented as mean ± SD, n = 3. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus PDGF-BB (-) Eup (-) group; * p < 0.05 and ** p < 0.01 versus PDGF-BB (+) Eup (-) group.

Journal: Pharmaceuticals

Article Title: Eupatorium lindleyanum DC Ameliorates Carbon Tetrachloride-Induced Hepatic Inflammation and Fibrotic Response in Mice

doi: 10.3390/ph18081228

Figure Lengend Snippet: Eup suppresses PDGF-BB-induced HSC activation by inhibiting the PDGF-BB/PDGFR-β signaling pathway. ( A ) LX-2 cells were cultured with 20 ng/mL PDGF-BB, 1, 10, and 20 μg/mL Eup for 24 h. ( B – E ) qRT-PCR analysis of α-SMA , Col1 , Col3 , and LOX in LX-2 cells administrated with different concentrations of Eup. ( F ) Representative immunoblot images demonstrating protein expression of GAPDH, α-SMA, p-PDGFR-β, PDGFR-β, p-AKT, AKT, p-ERK, and ERK. ( G – J ) Expression levels of α-SMA and phosphorylation ratios of PDGFR-β (p-PDGFR-β/PDGFR-β), AKT (p-AKT/AKT), and ERK (p-ERK/ERK). The loading control was GAPDH. Data are presented as mean ± SD, n = 3. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus PDGF-BB (-) Eup (-) group; * p < 0.05 and ** p < 0.01 versus PDGF-BB (+) Eup (-) group.

Article Snippet: For Western blot analysis, primary antibodies against β-actin (1:2500, abs171598, Absin, Shanghai, China), α-SMA (1:2500, Proteintech Group, Wuhan, China), Collagen I (1:2000, Proteintech Group, Wuhan, China), PDGFR-β (1:1250, Proteintech Group, Wuhan, China), p-PDGFR-β (1:1000, Abcam, UK), GAPDH (1:1500, Servicebio, Wuhan, China), p-AKT (1:1000, Abcam, UK), AKT (1:1000, Abcam, UK), p-ERK (1:1500, Selleck Chemicals, Houston, TX, USA) and ERK (1:1000, Selleck Chemicals, Houston, TX, USA), were applied.

Techniques: Activation Assay, Cell Culture, Quantitative RT-PCR, Western Blot, Expressing, Phospho-proteomics, Control

The mechanism diagram of Eup in improving CCl 4 -induced liver fibrosis. Eup suppressed the PDGF-BB/PDGFR-β signaling pathway, thereby inhibiting HSCs activation, and then improving liver fibrosis induced by CCl 4 .

Journal: Pharmaceuticals

Article Title: Eupatorium lindleyanum DC Ameliorates Carbon Tetrachloride-Induced Hepatic Inflammation and Fibrotic Response in Mice

doi: 10.3390/ph18081228

Figure Lengend Snippet: The mechanism diagram of Eup in improving CCl 4 -induced liver fibrosis. Eup suppressed the PDGF-BB/PDGFR-β signaling pathway, thereby inhibiting HSCs activation, and then improving liver fibrosis induced by CCl 4 .

Article Snippet: For Western blot analysis, primary antibodies against β-actin (1:2500, abs171598, Absin, Shanghai, China), α-SMA (1:2500, Proteintech Group, Wuhan, China), Collagen I (1:2000, Proteintech Group, Wuhan, China), PDGFR-β (1:1250, Proteintech Group, Wuhan, China), p-PDGFR-β (1:1000, Abcam, UK), GAPDH (1:1500, Servicebio, Wuhan, China), p-AKT (1:1000, Abcam, UK), AKT (1:1000, Abcam, UK), p-ERK (1:1500, Selleck Chemicals, Houston, TX, USA) and ERK (1:1000, Selleck Chemicals, Houston, TX, USA), were applied.

Techniques: Activation Assay