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  Indian J Med Microbiol
 

Figure 5: Protection of H2O2-induced mitochondrial dysfunction by honokiol in HaCaT cells. HaCaT cells were treated with honokiol (10 μM) or NAC (10 μM) for 1 h, and then exposed to H2O2 (500 μM) for 24 h. (A) JC-1 fluorescence intensity was detected using a flow cytometer. (B) Cellular ATP concentrations were measured. (C) Cytochrome c levels by Western blotting analysis. COX W and actin serve as protein loading controls for the cytosol and mitochondria, respectively. All data are expressed as mean ± SD of triplicate determinations (*P < 0.05 compared with the control group; #P < 0.05 compared with the H2O2-treated group). M.F.: mitochondrial fraction; C.F.: cytosolic fraction; ATP: adenosine triphoaphate.

Figure 5: Protection of H<sub>2</sub>O<sub>2</sub>-induced mitochondrial dysfunction by honokiol in HaCaT cells. HaCaT cells were treated with honokiol (10 μM) or NAC (10 μM) for 1 h, and then exposed to H<sub>2</sub>O<sub>2</sub> (500 μM) for 24 h. (A) JC-1 fluorescence intensity was detected using a flow cytometer. (B) Cellular ATP concentrations were measured. (C) Cytochrome c levels by Western blotting analysis. COX W and actin serve as protein loading controls for the cytosol and mitochondria, respectively. All data are expressed as mean ± SD of triplicate determinations (*<i>P</i> < 0.05 compared with the control group; <sup>#</sup><i>P</i> < 0.05 compared with the H<sub>2</sub>O<sub>2</sub>-treated group). M.F.: mitochondrial fraction; C.F.: cytosolic fraction; ATP: adenosine triphoaphate.