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. 2011 Aug 25;2(8):e195. doi: 10.1038/cddis.2011.76

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Copyright © 2011 Macmillan Publishers Limited

This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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HSP32/HO-1 is the major mediator of celastrol's protective effect. (a) HSP32/HO-1 is required for the protective effect of celastrol. Utricles from both HSP70^−/− and HSP70^+/+ mice were treated with celastrol and the HSP32/HO-1 inhibitor ZnPPIX. Gentamicin resulted in significant hair cell death in utricles of both genotypes. Celastrol inhibited gentamicin-induced hair cell death in both HSP70^−/− and HSP70^+/+ utricles. ZnPPIX abolished the protective effect of celastrol in both HSP70^−/− and HSP70^+/+ utricles (1-way ANOVA F_1,29=26.35, P<0.0001). Asterisks indicate significance (P<0.05) by post hoc analysis. (b) HSP32/HO-1 inhibits aminoglycoside-induced hair cell death. Utricles were treated with the HSP32/HO-1 inducer CoPPIX. HSP32/HO-1 induction inhibited aminoglycoside-induced hair cell death (2-way ANOVA F_1,9=10.36, P<0.011). (c) HSP32/HO-1 inhibits aminoglycoside-induced JNK activation. Neomycin increased JNK activation, and this activation was inhibited by CoPPIX. (d) CO inhibits aminoglycoside-induced hair cell death. Utricles were treated with CORM2, a CO-releasing molecule. CORM2 partially inhibited neomycin-induced hair cell death (1-way ANOVA F_1,25=79.29, P<0.0001)