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MedChemExpress metformin met
Establishment of zebrafish cartilage injury and mouse OA models and therapeutic evaluation of antidiabetic drugs, including semaglutide. A. The diagrams show the Tg(col2a1a:dendra2-NTR) transgenic line and its labeling of mandibular cartilages, including Meckel's cartilage (M), palatoquadrate cartilage (Pq), and ceratohyal cartilage (Ch). B. The flowchart illustrates the process of cartilage injury and drug treatment in zebrafish: at 3.5 days post-fertilization (dpf), zebrafish larvae were exposed to 12 mM metronidazole (MTZ) for 20 h, followed by drug intervention, with phenotypic analysis performed 3 days later. C. Representative gross morphology of zebrafish in the MTZ/NTR-induced cartilage injury repair model. D. Confocal microscopy analysis showing the repair effects of different antidiabetic drugs on zebrafish cartilage injury (n = 10). The antidiabetic agents included <t>metformin</t> (Met), empagliflozin (Emp), rosiglitazone (Ros), gliclazide (Gli), and semaglutide (Se). Working concentrations were selected based on published doses and further refined in pilot assays to identify the highest effective concentration that did not cause overt toxicity or teratogenic effects. E. Experimental design of Se administration in wild-type (WT) mice with DMM-induced osteoarthritis (OA). F. Body weight changes in WT mice during treatment with low- or high-dose Se following destabilization of the medial meniscus (DMM) surgery (n = 6). G. Mechanical allodynia in each group of WT mice was assessed using the von Frey test during Se treatment after DMM surgery (n = 6). H. Effects of Se on pain-related behavior in OA mice, along with representative gait footprints from each group. I. Quantitative gait analysis based on H-track parameters, expressed as the ratio of right hindlimb to left hindlimb (RH/LH) (n = 6). J. Representative micro-computed tomography (micro-CT) images of knee joints from each group, including sagittal, coronal, and transverse reconstructions, illustrate overall subchondral bone alterations following Se treatment. K. Quantitative analysis of subchondral bone structural parameters derived from micro-CT images in (J), including subchondral bone plate (SBP) thickness, bone volume fraction (BV/TV), and trabecular thickness (Tb.Th) (n = 6). Scale bar represents 100 μm. Data are presented as the means ± SD. ns. Non-significant. ∗P value < 0.05. ∗∗P value < 0.01. ∗∗∗P value < 0.001.
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor <t>Met-12.</t> Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).
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Image Search Results


Establishment of zebrafish cartilage injury and mouse OA models and therapeutic evaluation of antidiabetic drugs, including semaglutide. A. The diagrams show the Tg(col2a1a:dendra2-NTR) transgenic line and its labeling of mandibular cartilages, including Meckel's cartilage (M), palatoquadrate cartilage (Pq), and ceratohyal cartilage (Ch). B. The flowchart illustrates the process of cartilage injury and drug treatment in zebrafish: at 3.5 days post-fertilization (dpf), zebrafish larvae were exposed to 12 mM metronidazole (MTZ) for 20 h, followed by drug intervention, with phenotypic analysis performed 3 days later. C. Representative gross morphology of zebrafish in the MTZ/NTR-induced cartilage injury repair model. D. Confocal microscopy analysis showing the repair effects of different antidiabetic drugs on zebrafish cartilage injury (n = 10). The antidiabetic agents included metformin (Met), empagliflozin (Emp), rosiglitazone (Ros), gliclazide (Gli), and semaglutide (Se). Working concentrations were selected based on published doses and further refined in pilot assays to identify the highest effective concentration that did not cause overt toxicity or teratogenic effects. E. Experimental design of Se administration in wild-type (WT) mice with DMM-induced osteoarthritis (OA). F. Body weight changes in WT mice during treatment with low- or high-dose Se following destabilization of the medial meniscus (DMM) surgery (n = 6). G. Mechanical allodynia in each group of WT mice was assessed using the von Frey test during Se treatment after DMM surgery (n = 6). H. Effects of Se on pain-related behavior in OA mice, along with representative gait footprints from each group. I. Quantitative gait analysis based on H-track parameters, expressed as the ratio of right hindlimb to left hindlimb (RH/LH) (n = 6). J. Representative micro-computed tomography (micro-CT) images of knee joints from each group, including sagittal, coronal, and transverse reconstructions, illustrate overall subchondral bone alterations following Se treatment. K. Quantitative analysis of subchondral bone structural parameters derived from micro-CT images in (J), including subchondral bone plate (SBP) thickness, bone volume fraction (BV/TV), and trabecular thickness (Tb.Th) (n = 6). Scale bar represents 100 μm. Data are presented as the means ± SD. ns. Non-significant. ∗P value < 0.05. ∗∗P value < 0.01. ∗∗∗P value < 0.001.

Journal: Journal of Orthopaedic Translation

Article Title: Semaglutide alleviates osteoarthritis independent of weight loss via GLP-1R–mediated activation of autophagy through AKT/mTOR inhibition

doi: 10.1016/j.jot.2026.101166

Figure Lengend Snippet: Establishment of zebrafish cartilage injury and mouse OA models and therapeutic evaluation of antidiabetic drugs, including semaglutide. A. The diagrams show the Tg(col2a1a:dendra2-NTR) transgenic line and its labeling of mandibular cartilages, including Meckel's cartilage (M), palatoquadrate cartilage (Pq), and ceratohyal cartilage (Ch). B. The flowchart illustrates the process of cartilage injury and drug treatment in zebrafish: at 3.5 days post-fertilization (dpf), zebrafish larvae were exposed to 12 mM metronidazole (MTZ) for 20 h, followed by drug intervention, with phenotypic analysis performed 3 days later. C. Representative gross morphology of zebrafish in the MTZ/NTR-induced cartilage injury repair model. D. Confocal microscopy analysis showing the repair effects of different antidiabetic drugs on zebrafish cartilage injury (n = 10). The antidiabetic agents included metformin (Met), empagliflozin (Emp), rosiglitazone (Ros), gliclazide (Gli), and semaglutide (Se). Working concentrations were selected based on published doses and further refined in pilot assays to identify the highest effective concentration that did not cause overt toxicity or teratogenic effects. E. Experimental design of Se administration in wild-type (WT) mice with DMM-induced osteoarthritis (OA). F. Body weight changes in WT mice during treatment with low- or high-dose Se following destabilization of the medial meniscus (DMM) surgery (n = 6). G. Mechanical allodynia in each group of WT mice was assessed using the von Frey test during Se treatment after DMM surgery (n = 6). H. Effects of Se on pain-related behavior in OA mice, along with representative gait footprints from each group. I. Quantitative gait analysis based on H-track parameters, expressed as the ratio of right hindlimb to left hindlimb (RH/LH) (n = 6). J. Representative micro-computed tomography (micro-CT) images of knee joints from each group, including sagittal, coronal, and transverse reconstructions, illustrate overall subchondral bone alterations following Se treatment. K. Quantitative analysis of subchondral bone structural parameters derived from micro-CT images in (J), including subchondral bone plate (SBP) thickness, bone volume fraction (BV/TV), and trabecular thickness (Tb.Th) (n = 6). Scale bar represents 100 μm. Data are presented as the means ± SD. ns. Non-significant. ∗P value < 0.05. ∗∗P value < 0.01. ∗∗∗P value < 0.001.

Article Snippet: All antidiabetic agents, including metformin (Met) (5 μM, HY-B0627), empagliflozin (Emp) (1 μM, HY-15409), rosiglitazone (Ros) (1 μM, HY-17386), gliclazide (Gli) (5 μM, HY-B0753), and semaglutide (Se) (0.5 μM, HY-114118), were purchased from MedChemExpress (MCE, USA).

Techniques: Transgenic Assay, Labeling, Confocal Microscopy, Concentration Assay, Micro-CT, Derivative Assay

The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor Met-12. Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).

Journal: International Journal of Molecular Sciences

Article Title: Synergistic Induction of Caspase-8-Mediated Leukaemic Cell Death by Fisetin and Pinocembrin

doi: 10.3390/ijms27125622

Figure Lengend Snippet: The effect of fisetin (10 and 20 µM) on Jurkat cell survival, measured using XTT assay. In the presence and absence of Fas receptor inhibitor Met-12. Data represented as mean ± SEM ( n = 3) Statistical analysis carried out using ANOVA followed by Tukey’s post hoc test for significance (* p < 0.05) (*** p < 0.001) (**** p < 0.0001).

Article Snippet: Cells were treated with the Fas inhibitor Met-12 (CAS No. 1242964-46-0, purchased from MedChemExpress, catalogue number HY-P6440) at concentration of 20 μM and fisetin at concentrations of 10 μM and 20 μM, and combination treatments consisting of MET + fisetin (20 + 10 μM and 20 μM + 20 μM).

Techniques: XTT Assay