262796.fig.001a
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262796.fig.001b
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262796.fig.001c
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262796.fig.001d
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262796.fig.001e
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Figure 1: Histological analysis shikonin-treated mouse skin and grouping of genes that are responsive to shikonin treatment. (a) The histological characteristics of acetone- (vehicle control), shikonin-, and TPA-treated skin were revealed by H&E staining. Test mice (3 animals per group) were topically treated with (1) 100 μL acetone, (2) shikonin (3.5 mM in 100 μL acetone), or (3) TPA (10 nM in 100 μL acetone) for 24 h. Black bars mark the thickness of the epidermal layer (Ep), dermis (De), subcutaneous layer (SL; also known as hypodermis), and hair follicles (HF). The dotted line in panel 3 indicates a terminally damaged boundary line between the epidermal (stratum spinosum) and dermal layers. (b) Shikonin-responsive genes in skin, as compared to acetone- (vehicle control) treated skin samples, were grouped according to their known molecular, cellular, or biochemical functions. Classified gene groups were then listed according to the abundance in number of responsive genes in skin tissue treated with shikonin for 4 or 24 h. (c) Structure of the naphthoquinone, shikonin. (d and e) GeneGo Pathway Maps processed by MetaCore software analysis. By comparing the [ value] of different gene-clustering groups, the top ten responsive processes with specific cellular or molecular functions were predicted for evaluating the effect of shikonin. The orange bars indicate the calculated values generated from 4 h (d) and 24 h (e) datasets, respectively.