sch 442416  (MedChemExpress)

Journal: Pharmaceuticals

Article Title: Fructose-1,6-Bisphosphate Reduces Chronic Constriction Injury Neuropathic Pain in Mice by Targeting Dorsal Root Ganglia Nociceptive Neuron Activation

doi: 10.3390/ph18050660

Figure Lengend Snippet: Figure 3. The analgesic effect of FBP on CCI-induced mechanical hyperalgesia is dependent on adenosine A1 and A2 receptors. (A) Schematic representation of experimental design in this figure; (B) Treatment with DPCPX (A1 receptor antagonist) via i.t. route; (C) Treatment with DPCPX (A1 receptor antagonist) via i.pl. route; (D) Treatment with SCH442416 (A2A receptor antagonist) via i.t. route; (E) Treatment with SCH442416 (A2A receptor antagonist) via i.pl. route. n = 5–6 mice per group per experiment. * p < 0.05 CCI vs. sham group; # p < 0.05 vs. CCI + vehicle group; ** p < 0.05 vs. CCI + FBP 300 mg/kg group. *** p < 0.05 vs. vehicle group and CCI + FBP 300 mg/kg group (Two-way ANOVA followed by Tukey’s post-test).

Article Snippet: SCH442416 (2-(2-Furanyl)-7-[3-(4-methoxyphenyl)propyl]-7H-pyrazolo [4,3- e][1,2,4]triazolo [1,5-c]pyrimidin-5-amine) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 0439) were obtained from Tocris Cookson (Ballwin, MO, USA).

Techniques:

Journal: Cell communication and signaling : CCS

Article Title: Inhibition of adenosine/A2A receptor signaling suppresses dermal fibrosis by enhancing fatty acid oxidation.

doi: 10.1186/s12964-025-02210-2

Figure Lengend Snippet: Fig. 5 A2A mediates FAO through regulating CPT1A expression. (A-B) Immunoblot analysis of CPT1A (A) and RT-qPCR analysis of CPT1A (B) in dermal fibroblasts treated with TGF-β, with or without 1–20 μM SCH442416, for 48 h. (C-D) Representative immunofluorescent staining of CPT1A (green) and VI MENTIN (red) (C), and quantification of VIMENTIN+ CPT1A+ cells in the skin tissues from HC and SSc patients (D) (n = 5, scale bar: 20 μm). (E-F) Immunoblot analysis of fibronectin and α-SMA (E), and RT-qPCR analysis of COL1A1, COL1A2 and FN1 mRNA (F), in dermal fibroblasts treated with TGF-β, SCH442416 (10μM), and etomoxir (5μM) for 48 h. (G) RT-qPCR analysis of CPT1A mRNA in dermal fibroblasts after silencing of CPT1A. (H-I) Immunoblot analysis of fibronectin, α-SMA and CPT1A (H), and RT-qPCR analysis of ACTA2 and FN1 mRNA (I), in dermal fibroblasts after silencing of CPT1A and incubation with TGF-β for 48 h. (J-K) Immunoblot analysis of fibronectin and α-SMA (J), and RT-qPCR analysis of ACTA2 and FN1 mRNA (K), in dermal fibroblasts after silenc ing of CPT1A and incubation with TGF-β and SCH442416 (10μM) for 48 h. RT-qPCR results were normalized against GAPDH. Error bars represent mean +/- SD range. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; HC, healthy control

Article Snippet: For primary dermal fibroblasts treatment, cells were first starved in serum-free medium containing 0.1% FBS for 16 h, then treated with the following reagents as specified in each experiment, unless stated otherwise: TGF-β (10ng/ml, Peprotech, 100 −21), IL-1β (20 ng/ml, Peprotech, 200-01B), IL-4 (20 ng/ml, Peprotech, 200-04), IL-6 (20 ng/ml, Peprotech, 200-06), IL-12 (20 ng/ml, Peprotech, 200-12), CGS21680 (10μM, MCE, HY13201A), SCH442416 (10μM, Tocris, 2463), etomoxir (5 μM, Selleck, S8244), forskolin (30μM, Sigma, 344270), IVA337 (20 μM, Selleck, S8770) and 666 −15 (0.1 μM, MCE, HY101120).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, Staining, Incubation, Control

Journal: Cell communication and signaling : CCS

Article Title: Inhibition of adenosine/A2A receptor signaling suppresses dermal fibrosis by enhancing fatty acid oxidation.

doi: 10.1186/s12964-025-02210-2

Figure Lengend Snippet: Fig. 6 A2A regulates CPT1A expression via p-CREB/CREB pathway. (A) Immunoblot analysis of p-CREB and CREB in dermal fibroblasts treated with TGF-β, with or without SCH442416 (10μM), for 48 h. (B-C) Immunoblot analysis of p-CREB, CREB, fibronectin and CPT1A (B); and RT-qPCR analysis of COL1A1, FN1 and CPT1A (C) in dermal fibroblasts pretreated with or without forskolin (30μM, 30 min), followed by stimulation with or without TGF-β for 48 h. (D-E) Im munoblot analysis of p-CREB, CREB, fibronectin and CPT1A (D); and RT-qPCR analysis of COL1A1, FN1 and CPT1A (E) in dermal fibroblasts pretreated with or without forskolin, followed by stimulation with or without TGF-β and SCH442416 (10μM) for 48 h. (F-G) Immunoblot analysis of p-CREB, CREB, fibronectin and CPT1A (F), and RT-qPCR analysis of COL1A1, FN1 and CPT1A (G) in dermal fibroblasts treated with TGF-β, CGS21680 (10μM), and 666 − 15 (0.1μM) for 48 h. RT-qPCR results were normalized against GAPDH. Error bars represent mean +/- SD range. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; HC, healthy control

Article Snippet: For primary dermal fibroblasts treatment, cells were first starved in serum-free medium containing 0.1% FBS for 16 h, then treated with the following reagents as specified in each experiment, unless stated otherwise: TGF-β (10ng/ml, Peprotech, 100 −21), IL-1β (20 ng/ml, Peprotech, 200-01B), IL-4 (20 ng/ml, Peprotech, 200-04), IL-6 (20 ng/ml, Peprotech, 200-06), IL-12 (20 ng/ml, Peprotech, 200-12), CGS21680 (10μM, MCE, HY13201A), SCH442416 (10μM, Tocris, 2463), etomoxir (5 μM, Selleck, S8244), forskolin (30μM, Sigma, 344270), IVA337 (20 μM, Selleck, S8770) and 666 −15 (0.1 μM, MCE, HY101120).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, Control