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The goals of this study were to investigate the effects of hypoxia on cochlear hair cell damage, and to explore the role of sirtuin1 in hypoxia-induced hair cell damage. Cochlear organotypic cultures from postnatal day 4 rats were used in this study. Hypoxia was induced by treating cochlear explants with CoCl 2 . Cochlear cultures were treated with CoCl 2  alone or in combination with the sirtuin1 activator resveratrol and the sirtuin1 inhibitor sirtinol. Hair cell damage was identified by phalloidin staining and imaged using scanning electron microscopy. RT-PCR and Western blot analyses were used to detect the expression of sirtuin1 and acetylated nuclear factor-κB (NF-κB). Low concentrations of CoCl 2  (100–200 μM) did not cause an obvious change in the number and morphology of hair cells, whereas higher concentrations of CoCl 2  (300–400 μM) induced swelling of hair cells, accompanied by cell loss. Increased sirtuin1 expression was induced by CoCl 2  at 100 to 200 μM, but not at 400 μM. NF-κB acetylation was significantly increased in explants treated with 400 μM CoCl 2 . Pretreatment with resveratrol prevented CoCl 2 -induced hair cell loss and acetylation of NF-κB. The protective effect of resveratrol was significantly reduced by sirtinol. CoCl 2  induces hair cell damage in organotypic cochleae cultures. Resveratrol attenuates CoCl 2 -induced cochlear hair cell damage possibly via activation of sirtuin1, which deacetylates NF-κB.

Resveratrol Attenuates CoCl2-Induced Cochlear Hair Cell Damage through Upregulation of Sirtuin1 and NF-κB Deacetylation