| Literature DB >> 32918982 |
Yun Yeong Lee1, Oak-Sung Choo1, Yeon Ju Kim1, Eun Sol Gil2, Jeong Hun Jang1, Yup Kang3, Yun-Hoon Choung4.
Abstract
It is known that hyperlipidemia is a risk factor for sensorineural hearing loss. However, the biological mechanisms underlying hyperlipidemia and hearing impairment have not been completely elucidated in the cochlea. Based on our previous study of human subjects, elderly people taking drugs for hyperlipidemia showed better hearing than those not taking any medications. We hypothesized that drugs for hyperlipidemia, such as statins, may have the potential to prevent hearing impairment. The aim of this study was to investigate the correlation between hyperlipidemia and hearing impairment and the hearing preservation effect of atorvastatin using a hyperlipidemic mouse model with diet-induced obesity (DIO). Here, we demonstrate that DIO mice had a significant hearing impairment as well as increased levels of reactive oxygen species (ROS) and hair cell death due to reduced levels of pAKT and superoxide dismutase 2 (SOD2). However, these changes were significantly prevented by atorvastatin. Oxidative stress-induced intrinsic apoptosis was decreased by the high expression of Nrf2 and antioxidant genes, which improved mitochondrial function and ROS via activation of the PI3K-pAKT pathway by atorvastatin. Therefore, atorvastatin has the potential to prevent hearing impairment via redox balance in the presence of hyperlipidemia.Entities:
Keywords: Apoptosis; Atorvastatin; Hearing impairment; Hyperlipidemia; ROS; pAKT
Year: 2020 PMID: 32918982 DOI: 10.1016/j.bbamcr.2020.118850
Source DB: PubMed Journal: Biochim Biophys Acta Mol Cell Res ISSN: 0167-4889 Impact factor: 4.739