TY - JOUR T1 - Bisdemethoxycurcumin-mediated Attenuation of Apoptosis Prevents Gentamicin-induced Ototoxicity in Mouse Cochlear UB/OC-2 Cells JF - In Vivo JO - In Vivo SP - 1095 LP - 1105 DO - 10.21873/invivo.12807 VL - 36 IS - 3 AU - TING-YA KANG AU - CHUAN-JEN HSU AU - JIA-NI LIN AU - CHEN-CHI WU AU - JEN-SHU WANG AU - HUI-YI LIN AU - SZU-HUI YU AU - RONG-SHUAN WU AU - YU-HSUAN WEN AU - GUO-FANG TSENG AU - HUNG-PIN WU Y1 - 2022/05/01 UR - http://iv.iiarjournals.org/content/36/3/1095.abstract N2 - Background/Aim: Gentamicin has been widely prescribed since the last two decades despite its ototoxicity and nephrotoxicity. Bisdemethoxycurcumin (BDMC) is an affordable and safe curcuminoid with medicinal properties. We aimed to understand the effects of BDMC on the gentamicin-induced hair cell damage in mouse cochlear UB/OC-2 cells, in order to elucidate the therapeutic potential of BDMC against gentamicin-induced ototoxicity. Materials and Methods: We quantified the cell membrane potential and examined the regulators and cascade proteins in the intrinsic pathway of hair cell apoptosis. Mouse cochlear UB/OC-2 cells were treated with BDMC before exposure to gentamicin. The effects of BDMC on hair cell viability, mitochondrial function, and apoptosis-related proteins were examined by flow cytometry, western blot, and fluorescent staining. Results: Our results revealed that BDMC reversed gentamicin-mediated cycle arrest at the G2/M phase, stabilizing the mitochondrial membrane potential, decreasing cleaved caspase proteins, and successfully reversing hair cell apoptosis. Conclusion: BDMC is a potential agent for reducing gentamicin-induced ototoxicity. ER -