Baicalin attenuates gentamicin ‐induced cochlear hair cell ototoxicity

AbstractGentamicin can lead to cochlear hair cells associated ototoxicity by inducing apoptosis and oxidative stress, which can be alleviated by baicalin, one flavonoid extracted from the root ofScutellaria baicalensis. The role of baicalin in protecting gentamicin ‐induced hearing loss is unclear. Interference with oxidative stress was investigated in this study using House Ear Institute‐Organ of Corti1 (HEI‐OC1) cells, which were simultaneously treated with baicalin (0‐400 μm) and gentamicin (0.2 or 1  mm). MTT was used to assay cell viability and apoptosis was detected with Annexin V ‐fluorescein isothiocyanate staining. The production of reactive oxygen species was indicated by 2,7‐dichlorofluorescein diacetate fluorescence intensity and mitochondrial depolarization was assayed by JC1‐mitochondrial membrane potential assay. Poly(ADP‐ribose) polymerase (PARP), cleaved‐ caspase 3 and cleaved‐PARP expression were analyzed with western blot. Baicalin improved the viability of HEI‐OC1 cells and significantly reduced the oxidative stress and mitochondrial depolarization compared with the gentamicin treatment group. Gentamicin treatment increased the activation of P ARP and caspase‐3, while such an increase could be downregulated by baicalin. Baicalin attenuates gentamicin‐induced cochlear hair cells ototoxicity, and such inhibition may be mediated by the regulation of reactive oxygen species production, mitochondrial depolarization, and caspase‐3 ...
Source: Journal of Applied Toxicology - Category: Toxicology Authors: Tags: RESEARCH ARTICLE Source Type: research