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Melatonin protects cochlear hair cells from nicotine‐induced injury through inhibiting apoptosis, inflammation, oxidative stress and endoplasmic reticulum stress
Author(s) -
Zhou Xinjia,
Gao Yuan,
Hu Yue,
Ma Xiulan
Publication year - 2021
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13638
Subject(s) - endoplasmic reticulum , melatonin , oxidative stress , apoptosis , nicotine , inflammation , unfolded protein response , pharmacology , organ of corti , chemistry , hair cell , microbiology and biotechnology , medicine , endocrinology , biology , biochemistry , inner ear , anatomy
Hearing loss positively links with cigarette smoking. However, the involved mechanism and treatment strategies are largely unrevealed. This study aimed to investigate the damaging effect of nicotine on cochlear hair cells, reveal the underlying mechanism and evaluate the therapeutic effect of melatonin on nicotine‐induced injury. The results showed that nicotine induced cytotoxicity of House Ear Institute‐Organ of Corti 1 (HEI‐OC1) cochlear hair cells in a dose‐dependent manner (0, 2.5, 5, 10, 20, 40 and 80 μM). Functional investigations showed that nicotine (10 μM) stimulation dramatically promoted apoptosis, inflammatory response, oxidative stress and endoplasmic reticulum stress in HEI‐OC1 cells. Moreover, melatonin treatment dose‐dependently alleviated the nicotine‐induced cytotoxicity in HEI‐OC1 cells (0, 10 25, 50 and 100 μM). Further investigation showed that melatonin (100 μM) effectively attenuated the nicotine‐induced apoptosis, inflammation, oxidative stress and endoplasmic reticulum stress in HEI‐OC1 cells. Collectively, we demonstrated that nicotine induced apoptosis, inflammation, oxidative stress and endoplasmic reticulum stress of cochlear hair cells in an in vitro cell model. Melatonin showed protective effect on these aspects, suggesting that melatonin may be a potential agent for treating smoking‐induced hearing loss.