RT Journal Article
SR Electronic
T1 Bisdemethoxycurcumin-mediated Attenuation of Apoptosis Prevents Gentamicin-induced Ototoxicity in Mouse Cochlear UB/OC-2 Cells
JF In Vivo
JO In Vivo
FD International Institute of Anticancer Research
SP 1095
OP 1105
DO 10.21873/invivo.12807
VO 36
IS 3
A1 TING-YA KANG
A1 CHUAN-JEN HSU
A1 JIA-NI LIN
A1 CHEN-CHI WU
A1 JEN-SHU WANG
A1 HUI-YI LIN
A1 SZU-HUI YU
A1 RONG-SHUAN WU
A1 YU-HSUAN WEN
A1 GUO-FANG TSENG
A1 HUNG-PIN WU
YR 2022
UL http://iv.iiarjournals.org/content/36/3/1095.abstract
AB 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.