Figure 1. Isolation scheme of A. pectinifera.
Figure 2. Chemical structure of compound 1, 2, and 3.
Figure 3. Effect of compound 1, 2, and 3 on keratinocyte stem cells (KSCs) viability. After KSCs were treated with various concentrations of compound 1, 2, and 3 for 24 h, CCK-8 assay was performed. Data are shown as a percentage of control from three independent experiments in triplicate. *p < 0.05, ** p < 0.01 compared with the untreated control.
Figure 4. Effect of compound 1, 2, and 3 on proliferation of keratinocyte stem cells (KSCs). Cells were incubated with various concentration of compound 1, 2, and 3 for 72 h. KSCs proliferation was measured using CCK-8 assay. Data are shown as a percentage of control from the three independent experiments in triplicate and values represent as the mean ± SD. *p < 0.05, ** p < 0.01 compared with the untreated control (BM, basal medium). Growth medium (GM) was used as a positive control.
Figure 5. Transcriptional expression profile of HAS-2 and HAS-3 in compound 3-treated HaCaT cells. HaCaT cells were incubated with compound 3 for 24h. Total RNA was extracted and quantitative real time PCR was performed for HAS-2 (A) and HAS-3 (B). G3PDH was used as an internal control. Results are the mean ± SD. of experiments using data are shown as fold increase from the three independent experiments in triplicate. *p < 0.05, ** p < 0.01 compared with the untreated control. Retinoic acid (10-7 M) was used as a positive control.
Figure 6. Collagen synthesis-promoting effects of compound 3. Collagen synthesis was evaluated using pro-collagen EIA assay. TGF-β (10 ng/mL) was used as a positive control. *p < 0.05, ** p < 0.01 compared with the untreated control.
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