Baicalin attenuates gentamicin‐induced cochlear hair cell ototoxicity

Abstract

Gentamicin 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 of Scutellaria 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 PARP 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 and PARP activation.

Protective mechanism of ferulic acid against neomycin‐induced ototoxicity in zebrafish

“…44 The protective effects of other bioactive compounds were also explored in gentamicin-and neomycininduced hair cells damage in vitro and in vivo. [45][46][47][48] Collectively, those results indicated a protective role of FA on attenuating oxidative stress and apoptosis induced by neomycin ototoxicity in hair cells.…”

Puerarin alleviates the ototoxicity of gentamicin by inhibiting the mitochondria‑dependent apoptosis pathway

“…The mice in the PU group were intraperitoneally injected with 100 mg/kg PU (Sigma-Aldrich; Merck KGaA) once a day for 10 days (19). The mice in the GM group were first intraperitoneally injected with 1 ml physiological saline once a day for 3 consecutive days and then intraperitoneally injected with 200 mg/kg GM (Sigma-Aldrich; Merck KGaA) once a day for 7 days (20). The mice in the GM + PU group were first intraperitoneally injected with 100 mg/kg PU once a day for 3 consecutive days and then intraperitoneally injected with 100 mg/kg PU and 200 mg/kg GM once a day for 7 consecutive days.…”

Protective role of pyrroloquinoline quinone against gentamicin induced cochlear hair cell ototoxicity

“…Gentamicin (GM), one of the commonly used aminoglycosides antibiotics, usually causes ototoxicity, which damages the HCs on the basement membrane of the inner ear leading to hearing loss, tinnitus, and vestibular disorders (Xie et al, 2011). The ototoxicity can cause irreversible hearing loss, and repeated exposure to aminoglycosides can lead to additive damage to HCs and other structures and subsequently to deafness (Rybak & Ramkumar, 2007; Zhang & Yu, 2019). Although the protective effect on aminoglycoside ototoxicity has been studied, there is still no effective and recognized treatment.…”