Journal: Journal of Pharmaceutical Analysis

Article Title: Synergistic effects of methyl 2-cyano-3,11-dioxo-18beta-olean-1,-12-dien-30-oate and erlotinib on erlotinib-resistant non-small cell lung cancer cells

doi: 10.1016/j.jpha.2021.06.002

Figure Lengend Snippet: Cell viability summary showing calculated IC 50 values following 48 h treatment with various tyrosine kinase inhibitors in both HCC827 and HCC827R cells.

Article Snippet: ERL, tivantinib, dasatinib, osimertinib, olmutinib, crizotinib, and cabozantinib were purchased from MedChemExpress LLC (Princeton, NJ, USA).

Techniques:

Journal: Journal of Pharmaceutical Analysis

Article Title: Synergistic effects of methyl 2-cyano-3,11-dioxo-18beta-olean-1,-12-dien-30-oate and erlotinib on erlotinib-resistant non-small cell lung cancer cells

doi: 10.1016/j.jpha.2021.06.002

Figure Lengend Snippet: Cell viability summary showing calculated IC 50 values following simultaneous 48 h treatment with various tyrosine kinase inhibitors in combination with a constant concentration of 2 μM CDODA-Me in both HCC827 and HCC827R cells.

Article Snippet: ERL, tivantinib, dasatinib, osimertinib, olmutinib, crizotinib, and cabozantinib were purchased from MedChemExpress LLC (Princeton, NJ, USA).

Techniques: Concentration Assay

Journal: Experimental and Therapeutic Medicine

Article Title: mTORC1 is a key regulator that mediates OGD- and TGFβ1-induced myofibroblast transformation and chondroitin-4-sulfate expression in cardiac fibroblasts

doi: 10.3892/etm.2022.11340

Figure Lengend Snippet: OGD and TGFβ1 induce Smad3 and PI3K/Akt/mTOR signaling in CFs. OGD + TGFβ1 induced phosphorylation of (A and B) Smad3, (C and D) Akt, (E and F) PRAS40 and (G and H) p70S6K was detected by western blotting and analyzed. Data are representative of four independent experiments. * P<0.05, ** P<0.01 and *** P<0.001. OGD, oxygen-glucose deprivation; CFs, cardiac fibroblasts; p-, phosphorylated.

Article Snippet: The contribution of the PI3K/Akt/mTOR signaling axis to OGD- and TGFβ1 stimulation-induced myofibroblast transformation and CSPG synthesis was investigated by evaluating the effect of highly selective inhibitors of critical components of the PI3K/Akt/mTOR axis: PI3K (cat. no. ZSTK474; MedChem Express), Akt (cat. no. MK2206; MedChem Express) and mTOR (cat. no. AZD8055; MedChem Express).

Techniques: Western Blot

Journal: Experimental and Therapeutic Medicine

Article Title: mTORC1 is a key regulator that mediates OGD- and TGFβ1-induced myofibroblast transformation and chondroitin-4-sulfate expression in cardiac fibroblasts

doi: 10.3892/etm.2022.11340

Figure Lengend Snippet: Representative images of CFs treated with DMSO, 1 µM ZSTK474, 1 µM MK2206 or 1 µM AZD8055 prior to stimulation with OGD + TGFβ1. Cells were immunostained for α-SMA (green) and nuclei were stained with DAPI (blue). Scale bar=100 µm. CFs, cardiac fibroblasts; OGD, oxygen-glucose deprivation; α-SMA, α-smooth muscle actin.

Article Snippet: The contribution of the PI3K/Akt/mTOR signaling axis to OGD- and TGFβ1 stimulation-induced myofibroblast transformation and CSPG synthesis was investigated by evaluating the effect of highly selective inhibitors of critical components of the PI3K/Akt/mTOR axis: PI3K (cat. no. ZSTK474; MedChem Express), Akt (cat. no. MK2206; MedChem Express) and mTOR (cat. no. AZD8055; MedChem Express).

Techniques: Staining

Journal: Experimental and Therapeutic Medicine

Article Title: mTORC1 is a key regulator that mediates OGD- and TGFβ1-induced myofibroblast transformation and chondroitin-4-sulfate expression in cardiac fibroblasts

doi: 10.3892/etm.2022.11340

Figure Lengend Snippet: Inhibition of the OGD + TGFβ1 induced mTOR pathway attenuates the expression of α-SMA and C4S in CFs. (CFs were preincubated with DMSO or increasing concentrations of AZD8055 prior to stimulation with OGD + TGFβ1. (A) Western blotting was used to detect and analyze expression levels of (B) p-Smad3(Ser425)/Smad3, (C) p-AKT(Ser473)/AKT and (D) p-p70S6K(Thr389)/p70S6K. Data are representative of three independent experiments. CFs were preincubated with DMSO or 1 µM AZD8055 prior to stimulation with OGD + TGFβ1 and expression levels of (E and F) α-SMA and (G) 2H6 (using conditioned media) assessed by western blotting and analyses. Data are representative of four independent experiments. * P<0.05, ** P<0.01 and *** P<0.001. CFs, cardiac fibroblasts; OGD, oxygen-glucose deprivation; α-SMA, α-smooth muscle actin; p-, phosphorylated.

Article Snippet: The contribution of the PI3K/Akt/mTOR signaling axis to OGD- and TGFβ1 stimulation-induced myofibroblast transformation and CSPG synthesis was investigated by evaluating the effect of highly selective inhibitors of critical components of the PI3K/Akt/mTOR axis: PI3K (cat. no. ZSTK474; MedChem Express), Akt (cat. no. MK2206; MedChem Express) and mTOR (cat. no. AZD8055; MedChem Express).

Techniques: Inhibition, Expressing, Western Blot

Journal: Brain Sciences

Article Title: Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model

doi: 10.3390/brainsci13040579

Figure Lengend Snippet: The effects of CCR5 antagonists (AZD-5672) administered intrathecally (i.t.) according to timeline ( A ), at doses of 0.5, 2, 4, and 15 µg/5 µL on mechanical ( B ) and thermal ( C ) hypersensitivity and the influence of AZD-5672 at a dose of 4 μg/5 μL plus morphine 2.5 μg/5 μL on mechanical ( E ) and thermal ( F ) hypersensitivity, administered according to timeline ( D ), 7 days after CCI in mice. The data are presented as the mean ± SEM (naive n = 5; CCI n = 8–10). The results were evaluated using one-way ANOVA followed by Bonferroni’s post hoc test for comparisons of selected pairs. * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate significant differences vs. V-treated group at each of the investigated time points: 1, 4, and 24 h for ( B , C ) graphs; * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate significant differences vs. V + W-treated group for ( E , F ) graphs ; ### p < 0.001 and && p < 0.01 indicates significant differences between the V + M- and AZD + M-treated groups for ( E , F ) graphs ; and p < 0.01 indicates significant differences between the AZD + W- and AZD + M-treated groups. Abbreviations: V: vehicle (DMSO); W: vehicle ( aqua pro injectione ); M: morphine; AZD: AZD -5672; CCI: chronic constriction injury of the sciatic nerve.

Article Snippet: A single i.t. administration of J113863 (CCR1 antagonist, at doses of 1, 15, 30, and 60 μg/5; μL cat. #2595, Tocris, Bristol, UK), TAK-220 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5; μL cat. #HY-19974/CS-5579, MedChemExpress, Monmouth Junction, NJ, USA), or AZD-5672 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5 μL cat. #HY-119101/CS-0068004, MedChemExpress) were administered once to CCI-exposed mice on Day 7, when mechanical and thermal hypersensitivity were fully developed.

Techniques:

Journal: Brain Sciences

Article Title: Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model

doi: 10.3390/brainsci13040579

Figure Lengend Snippet: Comparison of the effects of intrathecal (i.t.) administration of substances targeting CCR1 (J113863), CCR5 (TAK-220 or AZD-5672), and their combination (J11 + TAK-220 or J11 + AZD-5672) at a dose of 15 µg/5 µL (timeline ( A )) on mechanical and thermal hypersensitivity measured after 1 h ( B , C ) and after 4 h ( D , E ), 7 days after chronic CCI in mice. The data are presented as the mean ± SEM (naive n = 5; CCI n = 7–8). The results were evaluated using one-way ANOVA followed by Bonferroni’s post hoc test for comparisons of selected pairs. ● p < 0.05, ●● p < 0.01, and ●●● p < 0.001 indicate significant differences vs. J11-treated group; ♦ p < 0.05 and ♦♦♦ p < 0.001 indicate significant differences vs. TAK-treated group; ■ p < 0.05 indicates significant differences vs. AZD-treated group; and ▲ p < 0.05 indicates significant differences vs. J11 + TAK-treated group. Abbreviations: N: naive; V: vehicle (DMSO); J11: J113863; TAK: TAK-220; AZD: AZD -5672; CCI: chronic constriction injury of the sciatic nerve.

Article Snippet: A single i.t. administration of J113863 (CCR1 antagonist, at doses of 1, 15, 30, and 60 μg/5; μL cat. #2595, Tocris, Bristol, UK), TAK-220 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5; μL cat. #HY-19974/CS-5579, MedChemExpress, Monmouth Junction, NJ, USA), or AZD-5672 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5 μL cat. #HY-119101/CS-0068004, MedChemExpress) were administered once to CCI-exposed mice on Day 7, when mechanical and thermal hypersensitivity were fully developed.

Techniques: Comparison

Journal: Brain Sciences

Article Title: Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model

doi: 10.3390/brainsci13040579

Figure Lengend Snippet: Pharmacological modulation of chemokines from MIP-1 family (CCL3 and CCL9) via neutralizing antibodies and their receptors (CCR1 by J113863, CCR5 by TAK-220 or AZD -5672) reduces neuropathic pain symptoms and influences morphine analgesia—evidence from mice model evoked by chronic constriction injury of the sciatic nerve.

Article Snippet: A single i.t. administration of J113863 (CCR1 antagonist, at doses of 1, 15, 30, and 60 μg/5; μL cat. #2595, Tocris, Bristol, UK), TAK-220 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5; μL cat. #HY-19974/CS-5579, MedChemExpress, Monmouth Junction, NJ, USA), or AZD-5672 (CCR5 antagonist, at doses of 0.5, 2, 4, and 15 μg/5 μL cat. #HY-119101/CS-0068004, MedChemExpress) were administered once to CCI-exposed mice on Day 7, when mechanical and thermal hypersensitivity were fully developed.

Techniques: