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  Indian J Med Microbiol
 

Figure 3: Tyrosinase activity of galactomannan fraction using cellular (a) and enzymatic (b) assays. Cellular assay used melanocytes and cells were induced with phorbol myristate acetate (10 ng/mL) and treated with galactomannan fraction (5–150 μg/mL). Ascorbic acid (5 μg/mL; AA) was used as a reference agent. Cells without phorbol myristate acetate and sample were negative control (C.) and cells treated with phorbol myristate acetate only were positive control (C+). Enzymatic assay was conducted by using L.3,4.dihydroxyphenylalanine substrate, tyrosinase, and galactomannan fraction at various concentrations (5–150 μg/mL). Ascorbic acid (5 μg/mL; AA), quercetin (25 μg/mL; Q), and arbutin (10 μg/mL; A) were used as reference agents. Control (C) was L.3,4.dihydroxyphenylalanine and tyrosinase only. Data were shown as mean ± standard deviation from duplicate experiments. P < 0.05 against control

Figure 3: Tyrosinase activity of galactomannan fraction using cellular (a) and enzymatic (b) assays. Cellular assay used melanocytes and cells were induced with phorbol myristate acetate (10 ng/mL) and treated with galactomannan fraction (5–150 μg/mL). Ascorbic acid (5 μg/mL; AA) was used as a reference agent. Cells without phorbol myristate acetate and sample were negative control (C.) and cells treated with phorbol myristate acetate only were positive control (C+). Enzymatic assay was conducted by using L.3,4.dihydroxyphenylalanine substrate, tyrosinase, and galactomannan fraction at various concentrations (5–150 μg/mL). Ascorbic acid (5 μg/mL; AA), quercetin (25 μg/mL; Q), and arbutin (10 μg/mL; A) were used as reference agents. Control (C) was L.3,4.dihydroxyphenylalanine and tyrosinase only. Data were shown as mean ± standard deviation from duplicate experiments. <i>P</i> < 0.05 against control