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Fig. 6 Compounds decreased the glucose level in a diabetic zebrafish model: (A) Schematic representation of zebrafish diabetic model Tg(−1.2ins:htBidTE-ON; LR). Zebrafish insulin promoter was employed to drive the proapoptotic gene human truncated Bid (htBid) under the control of a TRE-based system. After incubation with doxycycline (Dox) and tebufenozide (Tbf), the htBid will express and cause β-cell apoptosis. The htBid will not express without incubation of Dox and Tbf (red cross). (B) Representative confocal images of the β-cell number from Tg(−1.2ins:htBidTE-ON; LR); Tg(−1.2ins:H2BmCherry) larvae treated with (tBid + Dox + Tbf) or without (tBid) doxycycline and tebufenozide β cells were indicated by the fluorescence of mCherry. Scale bars indicate 10 μm. (C) Total free glucose level of 6 dpf Tg(−1.2ins:htBidTE-ON; LR) treated with or without compounds. Total of 10 μM of each compound was added at 5 dpf after the β-cell ablation, and lasted for 24 h; then, their glucose levels were measured. WT: wild type. RGZ: rosiglitazone, which was used as positive control. The values shown are means ± SEM from three independent experiments. ** p < 0.01, and *** p < 0.001 via one-way ANOVA.