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MedChemExpress tetrachloro
Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen <t>species;</t> <t>JC-1,</t> <t>5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine</t> iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.
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Yeasen Biotechnology tetrachloro
Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen <t>species;</t> <t>JC-1,</t> <t>5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine</t> iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.
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Beyotime tetrachloro
Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen <t>species;</t> <t>JC-1,</t> <t>5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine</t> iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.
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Beyotime confocal microscopy 5
Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen <t>species;</t> <t>JC-1,</t> <t>5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine</t> iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.
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Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen species; JC-1, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.

Journal: Frontiers in Pharmacology

Article Title: Piroxicam accelerates diabetic foot ulcer healing via ERα-dependent mitochondrial protection and oxidative stress relief

doi: 10.3389/fphar.2026.1834818

Figure Lengend Snippet: Piroxicam alleviated mitochondrial oxidative stress and restored the mitochondrial function of HG-induced HaCaT cells. After 24 h of induction with HG (60 mM), HaCaT cells were treated with piroxicam (0, 1.2, 3.7, 11, 33, 100 nM) for 24 h. (A) The level of ROS within mitochondria was assessed using MitoSOX staining, and red fluorescence indicated mitochondrial superoxide (scale bar = 50 μm). (B) HaCaT cells were stained with JC-1 dye. Red fluorescence (JC-1 aggregates) indicated healthy mitochondria with a high MMP, while green fluorescence (JC-1 monomers) indicated mitochondrial membrane depolarization (scale bar = 50 μm). (C) The expression of mitochondrial respiratory chain complex proteins, including ATP5A1 (complex V), MT-CO2 (complex IV), UQCRC1 (complex III), SDHB (complex II), and NDUFB8 (complex I), of HaCaT cells was determined by Western blotting. (D) Quantitative analysis of protein levels of ATP5A1, MT-CO2, UQCRC1, SDHB, and NDUFB8 was performed. (E) The expression of mitochondrial dynamics-related proteins, including DRP1, MFN1, MFN2, and OPA1, was measured using Western blotting. (F) Quantitative analysis of protein levels of DRP1, MFN1, MFN2, and OPA1 was performed. (G) HaCaT cells were stained with MitoTracker and observed using a confocal microscope (scale bar = 10 μm). All data were presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001 compared to the 0 nM group ( n = 3). Abbreviations: HG, high glucose; SD, standard deviation; ROS, reactive oxygen species; JC-1, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide; MMP, mitochondrial membrane potential; ATP5A1, ATP synthase F1 subunit alpha; MT-CO2, mitochondrial-encoded cytochrome c oxidase 2; UQCRC1, ubiquinol-cytochrome c reductase core protein 1; SDHB, succinate dehydrogenase complex iron-sulfur subunit B; NDUFB8, NADH: ubiquinone oxidoreductase subunit B8; DRP1, dynamin-related protein 1; MFN1, mitofusin 1; MFN2, mitofusin 2; OPA1, optic atrophy 1.

Article Snippet: MMP was detected using a 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining probe (MedChemExpress, Monmouth Junction, NJ, United States) following the manufacturer’s instructions.

Techniques: Staining, Fluorescence, Membrane, Expressing, Western Blot, Microscopy, Standard Deviation