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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: HSP90 inhibitor 17AAG attenuates sevoflurane-induced neurotoxicity in rats and human neuroglioma cells via induction of HSP70

Fig. 2

17AAG attenuated sevoflurane-induced apoptosis and oxidative stress in cultured H4 cells. H4 cells were treated with either vehicle (CON) or 17AAG before exposure to air with or without 4.1% sevoflurane (SEV) for 6 h. Cells were analyzed by (a, b) Hoechst assay (× 400 magnification; scale bar, 50 μm), and (c, d) flow cytometry to evaluate apoptosis (lower right quadrant, early apoptosis; upper right quadrant, late apoptosis). e, f The expression of Bcl-2, Bax and cleaved caspase-3 protein in H4 cells was examined by Western blot, with β-actin as loading control. g, h The generation of reactive oxygen species (ROS) in H4 cells was labeled by a cell-permeable ROS-probe DCFH-DA. The fluorescent hydrolysis product, DCFH, was quantified by flow cytometry. CON, control. Representative of 3 independent experiments. n = 6. Mean ± SD, **P < 0.01 vs. CON, ## P < 0.01 vs. SEV by one-way ANOVA followed by Bonferroni multiple comparisons test

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