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Tocris selective inhibitor sb203580

Determination of Usp18 expression in the astrocytes following treatment with MAPKs inhibitors. ( a ) Western blot analysis of protein levels of phosphorylated ERK, JNK, P38 kinase and Usp18 after astrocyte treatment with 10 μM P38 <t>(SB203580),</t> ERK (PD98059) or JNK (SP600125) inhibitor in the presence of 1 μg/mL rD-DT for 24h. Quantities were normalized to endogenous GAPDH. ( b ) Quantification data as shown in ( a ). Error bars represent the SEM (*P < 0.05). ( c ) RT-PCR analysis of Usp18 expression in the astrocytes with the same treatment. Experiments were performed at least in triplicates. Error bars represent the SEM (*P < 0.05).

Selective Inhibitor Sb203580, supplied by Tocris, used in various techniques. Bioz Stars score: 96/100, based on 1001 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Usp18 Mediates D-Dopachrome Tautomerase-Induced Astrocytic Inflammation After Spinal Cord Injury"

Article Title: Usp18 Mediates D-Dopachrome Tautomerase-Induced Astrocytic Inflammation After Spinal Cord Injury

Journal: Journal of Inflammation Research

doi: 10.2147/JIR.S505433

Figure Legend Snippet: Determination of Usp18 expression in the astrocytes following treatment with MAPKs inhibitors. ( a ) Western blot analysis of protein levels of phosphorylated ERK, JNK, P38 kinase and Usp18 after astrocyte treatment with 10 μM P38 (SB203580), ERK (PD98059) or JNK (SP600125) inhibitor in the presence of 1 μg/mL rD-DT for 24h. Quantities were normalized to endogenous GAPDH. ( b ) Quantification data as shown in ( a ). Error bars represent the SEM (*P < 0.05). ( c ) RT-PCR analysis of Usp18 expression in the astrocytes with the same treatment. Experiments were performed at least in triplicates. Error bars represent the SEM (*P < 0.05).

Techniques Used: Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction

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Journal: Journal of Inflammation Research

Article Title: Usp18 Mediates D-Dopachrome Tautomerase-Induced Astrocytic Inflammation After Spinal Cord Injury

doi: 10.2147/JIR.S505433

Figure Lengend Snippet: Determination of Usp18 expression in the astrocytes following treatment with MAPKs inhibitors. ( a ) Western blot analysis of protein levels of phosphorylated ERK, JNK, P38 kinase and Usp18 after astrocyte treatment with 10 μM P38 (SB203580), ERK (PD98059) or JNK (SP600125) inhibitor in the presence of 1 μg/mL rD-DT for 24h. Quantities were normalized to endogenous GAPDH. ( b ) Quantification data as shown in ( a ). Error bars represent the SEM (*P < 0.05). ( c ) RT-PCR analysis of Usp18 expression in the astrocytes with the same treatment. Experiments were performed at least in triplicates. Error bars represent the SEM (*P < 0.05).

Article Snippet: To examine the effects of D-DT on the expression of Usp18, the primary astrocytes were treated with various selective inhibitor SB203580 (TOCRIS), SP600125 (TOCRIS) or PD98059 (TOCRIS) in the presence or absence of 1 μg/mL recombinant D-DT (Aviva Systems Biology) for 24 h prior to biochemical assay.

Techniques: Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction

Figure 1 Increased levels of phospho-FGFR1 in cardiomyocytes of diabetic mice. C57BL/6 mice were made diabetic by STZ. Heart tissues were harvested after 20 weeks of disease duration from diabetic (STZ) and non-diabetic control (Ctrl) mice. (A, B) Representative site-speciﬁc tyrosine kinase phosphorylation PST228 ProArray showing phosphorylated proteins (A). Magniﬁed images and signal-to-noise ratio (SNR) of FGFR1 (Tyr766) in STZ (red box) and Ctrl (yellow box) are shown in panel (B). (C) Relative abundance of FGFR1 protein in STZ and Ctrl heart tissues from AVK276 Kinase Array were shown. (D) Representative blots showing the levels of p-FGFR1 (Tyr-766) and FGFR1 in heart tissue. GAPDH was used as a loading control. (E) Immunoﬂuorescence staining of mouse heart tissues for p-FGFR1 (red), FGFR1 (red), and a-actinin (green). Sections were counterstained with DAPI (blue). Arrows showing p-FGFR1-positive cells (Scale bar Z 50 mm). (F) Levels of p-FGFR1 (Tyr-766) and FGFR1 in primary adult mouse cardiomyocytes and cardiac ﬁbroblasts. Cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control. (G) Levels of p-FGFR1 (Tyr-766) and FGFR1 in rat primary cardiomyocytes. Isolated cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control.

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 1 Increased levels of phospho-FGFR1 in cardiomyocytes of diabetic mice. C57BL/6 mice were made diabetic by STZ. Heart tissues were harvested after 20 weeks of disease duration from diabetic (STZ) and non-diabetic control (Ctrl) mice. (A, B) Representative site-speciﬁc tyrosine kinase phosphorylation PST228 ProArray showing phosphorylated proteins (A). Magniﬁed images and signal-to-noise ratio (SNR) of FGFR1 (Tyr766) in STZ (red box) and Ctrl (yellow box) are shown in panel (B). (C) Relative abundance of FGFR1 protein in STZ and Ctrl heart tissues from AVK276 Kinase Array were shown. (D) Representative blots showing the levels of p-FGFR1 (Tyr-766) and FGFR1 in heart tissue. GAPDH was used as a loading control. (E) Immunoﬂuorescence staining of mouse heart tissues for p-FGFR1 (red), FGFR1 (red), and a-actinin (green). Sections were counterstained with DAPI (blue). Arrows showing p-FGFR1-positive cells (Scale bar Z 50 mm). (F) Levels of p-FGFR1 (Tyr-766) and FGFR1 in primary adult mouse cardiomyocytes and cardiac ﬁbroblasts. Cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control. (G) Levels of p-FGFR1 (Tyr-766) and FGFR1 in rat primary cardiomyocytes. Isolated cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control.

Article Snippet: Selective FGFR1 inhibitor AZD4547 (S2801), p38 inhibitor SB203580 (S1076), ERK inhibitor SCH772984 (S7101), and JNK inhibitor SP600125 (S1460) were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Control, Phospho-proteomics, Staining, Isolation

Figure 2 Extracellular HG activates FGFR1 in cardiomyocytes by engaging TLR4. (A) H9C2 cells were exposed to 33 mmol/L glucose (HG). Levels of p-FGFR1 at Tyr-766 and total FGFR1 were determined at the indicated time points. GAPDH was used as a loading control. (B) Schematic illustrating the potential modes by which HG may activate FGFR1, including intracellular activation following uptake of glucose through GLUT4/GLUT1 (1) and RAGE (2) or extracellular activation (3). (C) Representative immunoblots showing levels of GLUT4 in H9C2 cells transfected with GLUT4 siRNA. GAPDH was used as a loading control. (D) Levels of p-FGFR1 induced by a 15-min HG exposure of H9C2 cells with or without GLUT4 siRNA. GAPDH was used as a loading control. (E) SPR analysis showing no direct interaction between rhFGFR1 and glucose. (F) HEK-293T cells were transfected with full-length FGFR1 (His-tagged) or truncated FGFR1 (D22e376). Cells were exposed to HG for 15 min. Levels of p-FGFR1 and His-tag were measured by immunoblotting. (G) Schematic illustrating the possible involvement of TLR4 in FGFR1 activation by HG. (H) Heart tissue lysates from diabetic (STZ) and non-diabetic (Ctrl) were used to immunoprecipitate c-Src (IP). Immunoblotting (IB) for FGFR1 was then performed. (I) H9C2 cells were exposed to HG for up to 15 min. Protein levels of p-c-Src/c-Src were determined. GAPDH was used as a loading control. (JeL) Levels of FGFR1 (J), c-Src (K), and TLR4 (L) in H9C2 cells transfected with targeting siRNA. (M) H9C2 cells transfected with FGFR1 or c-Src siRNA were exposed to HG for 15 min. Levels of p-FGFR1 (Tyr-766) and p-c-Src were measured. (N) H9C2 transfected with TLR4 siRNA were exposed to HG for 15 min. Lysates were probed for p-FGFR1 and p-c-Src. (O) H9C2 cells were transfected with TLR4 siRNA and exposed to HG for 15 min. Lysates from cells were immunoprecipitated with p-c-Src antibody and probed for p-FGFR1.

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 2 Extracellular HG activates FGFR1 in cardiomyocytes by engaging TLR4. (A) H9C2 cells were exposed to 33 mmol/L glucose (HG). Levels of p-FGFR1 at Tyr-766 and total FGFR1 were determined at the indicated time points. GAPDH was used as a loading control. (B) Schematic illustrating the potential modes by which HG may activate FGFR1, including intracellular activation following uptake of glucose through GLUT4/GLUT1 (1) and RAGE (2) or extracellular activation (3). (C) Representative immunoblots showing levels of GLUT4 in H9C2 cells transfected with GLUT4 siRNA. GAPDH was used as a loading control. (D) Levels of p-FGFR1 induced by a 15-min HG exposure of H9C2 cells with or without GLUT4 siRNA. GAPDH was used as a loading control. (E) SPR analysis showing no direct interaction between rhFGFR1 and glucose. (F) HEK-293T cells were transfected with full-length FGFR1 (His-tagged) or truncated FGFR1 (D22e376). Cells were exposed to HG for 15 min. Levels of p-FGFR1 and His-tag were measured by immunoblotting. (G) Schematic illustrating the possible involvement of TLR4 in FGFR1 activation by HG. (H) Heart tissue lysates from diabetic (STZ) and non-diabetic (Ctrl) were used to immunoprecipitate c-Src (IP). Immunoblotting (IB) for FGFR1 was then performed. (I) H9C2 cells were exposed to HG for up to 15 min. Protein levels of p-c-Src/c-Src were determined. GAPDH was used as a loading control. (JeL) Levels of FGFR1 (J), c-Src (K), and TLR4 (L) in H9C2 cells transfected with targeting siRNA. (M) H9C2 cells transfected with FGFR1 or c-Src siRNA were exposed to HG for 15 min. Levels of p-FGFR1 (Tyr-766) and p-c-Src were measured. (N) H9C2 transfected with TLR4 siRNA were exposed to HG for 15 min. Lysates were probed for p-FGFR1 and p-c-Src. (O) H9C2 cells were transfected with TLR4 siRNA and exposed to HG for 15 min. Lysates from cells were immunoprecipitated with p-c-Src antibody and probed for p-FGFR1.

Techniques: Control, Activation Assay, Western Blot, Transfection, Immunoprecipitation

Figure 3 HG-induced FGFR1 activation leads to inﬂammatory injuries in cardiomyocytes. (A) Venn diagram of differentially expressed genes in H9C2 cells. H9C2 cells were transfected with or without FGFR1 siRNA. Cells were then exposed to HG for 8 h. RNA from Ctrl, HG, and HG þ siFGFR1 (n Z 3) was sequenced. (B) GO analysis showing FGFR1 regulated inﬂammatory response genes in H9C2 cells. The inﬂammation-related pathways were highlighted in red font. (C) mRNA levels of TNF-a and IL-6 in H9C2 cells exposed to HG for 6 h (mean SEM, n Z 3; ***P < 0.001). (D, E) H9C2 cells were transfected with FGFR1 siRNA and exposed to HG for 24 h. Lysates were probed for COL-1 (D), TGFb1 (D), b-MyHC (E), and ANP (E). GAPDH was used as loading control. (F) Rhodamine phalloidin staining of H9C2 cells, showing the effects of HG following FGFR1 knockdown. Cells were counterstained with DAPI (blue) (Scale bar Z 50 mm). (G) FGFR1-deleted (Fgfr1-KO) H9C2 cells were transfected with Flag-Fgfr1Y766A or Flag- Fgfr1WT. Cells were then exposed to HG for 15 min. Levels of p-FGFR1 and His-tag were measured by immunoblotting. (H, I) Fgfr1-KO H9C2 cells were prepared as in Panel (G) but exposed to HG for 24 h. Lysates from cells were probed for COL-1 (H), TGFb1 (H), b-MyHC (I), and ANP (I). (J) Rhodamine phalloidin staining of Fgfr1-KO H9C2 cells. Cells were prepared and treated as in Panel (H) (Scale bar Z 50 mm). (K) H9C2 cells were transfected with full-length FGFR1 (Lenti- Fgfr1) or empty vector (NC). Cells were then exposed to HG for 15 min. Levels of p-FGFR1 (Tyr 766) were measured by immunoblotting. Total FGFR1 and GAPDH were used as controls. (L) mRNA levels of TNF-a and IL-6 in H9C2 cells exposed to HG for 6 h (mean SEM, n Z 3; *P < 0.05, **P < 0.01, ***P < 0.005). (M, N) H9C2 cells were prepared as in Panel (K) but exposed to HG for 24 h. Lysates from cells were probed for COL-1 (M), TGF-b1 (M), b-MyHC (N), and ANP (N). (O) Rhodamine phalloidin staining of H9C2 cells. Treatment of cells was carried out as in Panel (M) (Scale bar Z 50 mm).

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 3 HG-induced FGFR1 activation leads to inﬂammatory injuries in cardiomyocytes. (A) Venn diagram of differentially expressed genes in H9C2 cells. H9C2 cells were transfected with or without FGFR1 siRNA. Cells were then exposed to HG for 8 h. RNA from Ctrl, HG, and HG þ siFGFR1 (n Z 3) was sequenced. (B) GO analysis showing FGFR1 regulated inﬂammatory response genes in H9C2 cells. The inﬂammation-related pathways were highlighted in red font. (C) mRNA levels of TNF-a and IL-6 in H9C2 cells exposed to HG for 6 h (mean SEM, n Z 3; ***P < 0.001). (D, E) H9C2 cells were transfected with FGFR1 siRNA and exposed to HG for 24 h. Lysates were probed for COL-1 (D), TGFb1 (D), b-MyHC (E), and ANP (E). GAPDH was used as loading control. (F) Rhodamine phalloidin staining of H9C2 cells, showing the effects of HG following FGFR1 knockdown. Cells were counterstained with DAPI (blue) (Scale bar Z 50 mm). (G) FGFR1-deleted (Fgfr1-KO) H9C2 cells were transfected with Flag-Fgfr1Y766A or Flag- Fgfr1WT. Cells were then exposed to HG for 15 min. Levels of p-FGFR1 and His-tag were measured by immunoblotting. (H, I) Fgfr1-KO H9C2 cells were prepared as in Panel (G) but exposed to HG for 24 h. Lysates from cells were probed for COL-1 (H), TGFb1 (H), b-MyHC (I), and ANP (I). (J) Rhodamine phalloidin staining of Fgfr1-KO H9C2 cells. Cells were prepared and treated as in Panel (H) (Scale bar Z 50 mm). (K) H9C2 cells were transfected with full-length FGFR1 (Lenti- Fgfr1) or empty vector (NC). Cells were then exposed to HG for 15 min. Levels of p-FGFR1 (Tyr 766) were measured by immunoblotting. Total FGFR1 and GAPDH were used as controls. (L) mRNA levels of TNF-a and IL-6 in H9C2 cells exposed to HG for 6 h (mean SEM, n Z 3; *P < 0.05, **P < 0.01, ***P < 0.005). (M, N) H9C2 cells were prepared as in Panel (K) but exposed to HG for 24 h. Lysates from cells were probed for COL-1 (M), TGF-b1 (M), b-MyHC (N), and ANP (N). (O) Rhodamine phalloidin staining of H9C2 cells. Treatment of cells was carried out as in Panel (M) (Scale bar Z 50 mm).

Techniques: Activation Assay, Transfection, Control, Staining, Knockdown, Western Blot, Plasmid Preparation

Figure 4 NFkB links FGFR1 to downstream responses in HG-exposed cardiomyocytes. (A) TRRUST Transcription Factors analysis showing the top 10 protein-coding transcripts (ranked by adjusted P-value) that were increased by HG and suppressed by FGFR1 knockdown. (B) Immunoblot analysis of p-p65, p65, and IkBa in H9C2 cells. Cells were transfected with FGFR1 siRNA and then exposed to HG for 30 min. GAPDH was used as control. (C) Rat primary cardiomyocytes were pretreated with 5 mmol/L AZD4547 for 1 h and then exposed to 33 mmol/L HG for 30 min. Levels of p-p65, p65, and IkBa were measured, with GAPDH as control. (D) H9C2 cells were transfected with FGFR1 siRNA and then exposed to HG for 8 h. NFkB p65 antibody was used for ChIP. Candidate gene promoters (Tnfa and Il6) were detected by qPCR (mean SEM, n Z 3; *P < 0.05; **P < 0.01). (E) Fgfr1-KO H9C2 cells were transfected with Flag-Fgfr1Y766A or Flag-Fgfr1WT. Cells were then exposed to HG for 30 min. Levels of p-p65, p65, and IkBa were measured by immunoblotting with GAPDH as loading control. (F) H9c2 cells were prepared and treated as indicated in Panel (B). Levels of p-ERK1/2, p-JNK, and p-p38 were measured. Total proteins and GAPDH were used as controls. (G) Rat primary cardiomyocytes were pretreated with 5 mmol/L AZD4547 for 1 h and then exposed to 33 mmol/L HG for 30 min. Levels of p-ERK1/2, p-JNK, and p-p38 were measured. Total proteins and GAPDH were used as controls. (H, I) H9C2 cells were transfected with TLR4 siRNA (H) or c-Src siRNA (I) and then exposed to HG for 30 min. Lysates were probed for levels of phosphorylated MAPK pathway proteins. Total proteins and GAPDH were used as controls.

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 4 NFkB links FGFR1 to downstream responses in HG-exposed cardiomyocytes. (A) TRRUST Transcription Factors analysis showing the top 10 protein-coding transcripts (ranked by adjusted P-value) that were increased by HG and suppressed by FGFR1 knockdown. (B) Immunoblot analysis of p-p65, p65, and IkBa in H9C2 cells. Cells were transfected with FGFR1 siRNA and then exposed to HG for 30 min. GAPDH was used as control. (C) Rat primary cardiomyocytes were pretreated with 5 mmol/L AZD4547 for 1 h and then exposed to 33 mmol/L HG for 30 min. Levels of p-p65, p65, and IkBa were measured, with GAPDH as control. (D) H9C2 cells were transfected with FGFR1 siRNA and then exposed to HG for 8 h. NFkB p65 antibody was used for ChIP. Candidate gene promoters (Tnfa and Il6) were detected by qPCR (mean SEM, n Z 3; *P < 0.05; **P < 0.01). (E) Fgfr1-KO H9C2 cells were transfected with Flag-Fgfr1Y766A or Flag-Fgfr1WT. Cells were then exposed to HG for 30 min. Levels of p-p65, p65, and IkBa were measured by immunoblotting with GAPDH as loading control. (F) H9c2 cells were prepared and treated as indicated in Panel (B). Levels of p-ERK1/2, p-JNK, and p-p38 were measured. Total proteins and GAPDH were used as controls. (G) Rat primary cardiomyocytes were pretreated with 5 mmol/L AZD4547 for 1 h and then exposed to 33 mmol/L HG for 30 min. Levels of p-ERK1/2, p-JNK, and p-p38 were measured. Total proteins and GAPDH were used as controls. (H, I) H9C2 cells were transfected with TLR4 siRNA (H) or c-Src siRNA (I) and then exposed to HG for 30 min. Lysates were probed for levels of phosphorylated MAPK pathway proteins. Total proteins and GAPDH were used as controls.

Techniques: Knockdown, Western Blot, Transfection, Control

Figure 5 Cardiac-speciﬁc FGFR1 deﬁciency protects hearts in STZ-induced diabetic mice. Diabetes was induced in Fgfr1ﬂox and Fgfr1DCM

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 5 Cardiac-speciﬁc FGFR1 deﬁciency protects hearts in STZ-induced diabetic mice. Diabetes was induced in Fgfr1ﬂox and Fgfr1DCM

Techniques:

$Figure 6 Inhibition of FGFR1 by AZD4547 prevents cardiac injury in STZ-induced diabetic mice. Mice were made diabetic with STZ. FGFR1 was inhibited by treating mice with 5 mg/kg AZD4547 every other day. Heart tissues were examined at week 20 following the onset of diabetes (Ctrl, control group; STZ, type one diabetic group; STZ þ AZD, AZD4547-treated diabetic group; n Z 7 per group). (A, B) Weekly mea- surements showing levels of blood glucose (A) and body weights (B) in mice. (C) Ejection fraction values from the transthoracic echocardi- ography of the mice (mean SEM, n Z 7; *P < 0.05, ***P < 0.001). (D, E) Levels of BNP (D), CK-MB (E), and LDH (E) in blood samples of mice at the conclusion of the study (mean SEM, n Z 7; *P < 0.05, **P < 0.01). (F) Longitudinal and transversal H&E-stained sections of mouse hearts. (G) Heart sections were stained with Sirius Red (upper panel) and Masson’s Trichrome stain (lower panel) to assess ﬁbrotic changes. (H) Levels of COL-1, TGF-b1, b-MyHC, and ANP proteins in the heart tissues of mice were detected by immunoblotting. GAPDH was used as control. (I) Levels of pFGFR1 and FGFR1 in heart tissue lysates. GAPDH was used as control. (J) mRNA levels of TNF-a and IL-6 in heart tissues of mice (mean SEM, n Z 7; **P < 0.01, ***P < 0.001). (K) Levels of IkBa in heart tissue lysates. GAPDH was used as control. (L) MAPK pathway activation was determined by measuring levels of p-JNK, p-ERK, and p-p38. Total proteins and GAPDH were used as controls.$

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 6 Inhibition of FGFR1 by AZD4547 prevents cardiac injury in STZ-induced diabetic mice. Mice were made diabetic with STZ. FGFR1 was inhibited by treating mice with 5 mg/kg AZD4547 every other day. Heart tissues were examined at week 20 following the onset of diabetes (Ctrl, control group; STZ, type one diabetic group; STZ þ AZD, AZD4547-treated diabetic group; n Z 7 per group). (A, B) Weekly mea- surements showing levels of blood glucose (A) and body weights (B) in mice. (C) Ejection fraction values from the transthoracic echocardi- ography of the mice (mean SEM, n Z 7; *P < 0.05, ***P < 0.001). (D, E) Levels of BNP (D), CK-MB (E), and LDH (E) in blood samples of mice at the conclusion of the study (mean SEM, n Z 7; *P < 0.05, **P < 0.01). (F) Longitudinal and transversal H&E-stained sections of mouse hearts. (G) Heart sections were stained with Sirius Red (upper panel) and Masson’s Trichrome stain (lower panel) to assess ﬁbrotic changes. (H) Levels of COL-1, TGF-b1, b-MyHC, and ANP proteins in the heart tissues of mice were detected by immunoblotting. GAPDH was used as control. (I) Levels of pFGFR1 and FGFR1 in heart tissue lysates. GAPDH was used as control. (J) mRNA levels of TNF-a and IL-6 in heart tissues of mice (mean SEM, n Z 7; **P < 0.01, ***P < 0.001). (K) Levels of IkBa in heart tissue lysates. GAPDH was used as control. (L) MAPK pathway activation was determined by measuring levels of p-JNK, p-ERK, and p-p38. Total proteins and GAPDH were used as controls.

Techniques: Inhibition, Control, Staining, Western Blot, Activation Assay

$Figure 7 Inhibition of FGFR1 by AZD4547 prevents cardiac injury in db/db mice. FGFR1 was inhibited by treating db/db mice with 5 mg/kg AZD4547 every other day. Heart tissues were examined at Week 8 following AZD4547 treatment (db/m, control group; db/db, type 2 diabetic group; db/db þ AZD, AZD4547-treated diabetic group; n Z 6 per group). (A, B) Weekly measurements showing levels of blood glucose (A) and body weights (B) in mice. (C) Ejection fraction values from the transthoracic echocardiography of the mice (mean SEM, n Z 6; **P < 0.01, ***P < 0.001). (D, E) Levels of BNP (D), CK-MB (E), and LDH (E) in blood samples of mice at the conclusion of the study (mean SEM, n Z 6; *P < 0.05, **P < 0.01, ***P < 0.001). (F) Longitudinal and transversal H&E-stained sections of mouse hearts. (G) Heart sections were stained with Sirius Red (upper panel) and Masson’s Trichrome stain (lower panel) to assess ﬁbrotic changes. (H) Levels of COL-1, TGF-b1, b-MyHC, and ANP proteins in the heart tissues of mice were detected by immunoblotting. GAPDH was used as control. (I) Levels of pFGFR1 and FGFR1 in heart tissue lysates. GAPDH was used as control. (J) mRNA levels of TNF-a and IL-6 in heart tissues of mice (mean SEM, n Z 6; **P < 0.01, ***P < 0.001). (K) Levels of IkBa in heart tissue lysates. GAPDH was used as control. (L) MAPK pathway activation was determined by measuring levels of p-JNK, p-ERK, and p-p38. Total proteins and GAPDH were used as controls.$

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 7 Inhibition of FGFR1 by AZD4547 prevents cardiac injury in db/db mice. FGFR1 was inhibited by treating db/db mice with 5 mg/kg AZD4547 every other day. Heart tissues were examined at Week 8 following AZD4547 treatment (db/m, control group; db/db, type 2 diabetic group; db/db þ AZD, AZD4547-treated diabetic group; n Z 6 per group). (A, B) Weekly measurements showing levels of blood glucose (A) and body weights (B) in mice. (C) Ejection fraction values from the transthoracic echocardiography of the mice (mean SEM, n Z 6; **P < 0.01, ***P < 0.001). (D, E) Levels of BNP (D), CK-MB (E), and LDH (E) in blood samples of mice at the conclusion of the study (mean SEM, n Z 6; *P < 0.05, **P < 0.01, ***P < 0.001). (F) Longitudinal and transversal H&E-stained sections of mouse hearts. (G) Heart sections were stained with Sirius Red (upper panel) and Masson’s Trichrome stain (lower panel) to assess ﬁbrotic changes. (H) Levels of COL-1, TGF-b1, b-MyHC, and ANP proteins in the heart tissues of mice were detected by immunoblotting. GAPDH was used as control. (I) Levels of pFGFR1 and FGFR1 in heart tissue lysates. GAPDH was used as control. (J) mRNA levels of TNF-a and IL-6 in heart tissues of mice (mean SEM, n Z 6; **P < 0.01, ***P < 0.001). (K) Levels of IkBa in heart tissue lysates. GAPDH was used as control. (L) MAPK pathway activation was determined by measuring levels of p-JNK, p-ERK, and p-p38. Total proteins and GAPDH were used as controls.

Techniques: Inhibition, Control, Staining, Western Blot, Activation Assay

Figure 8 The role of FGFR1 in diabetic cardiomyopathy.

Journal: Acta pharmaceutica Sinica. B

Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes.

doi: 10.1016/j.apsb.2024.01.013

Figure Lengend Snippet: Figure 8 The role of FGFR1 in diabetic cardiomyopathy.

Techniques:

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