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Korean red ginseng ameliorates acute 3-nitropropionic acid-induced cochlear damage in mice

Authors :
Tian, Chunjie
Kim, Young Ho
Kim, Young Chul
Park, Kyung Tae
Kim, Seung Won
Kim, Youn Ju
Lim, Hye Jin
Choung, Yun-Hoon
Source :
NeuroToxicology. Jan2013, Vol. 34, p42-50. 9p.
Publication Year :
2013

Abstract

Abstract: 3-Nitropropionic acid (3-NP), a mitochondrial toxin, has been reported to induce an acute cochlear damage. Korean red ginseng (KRG) is known to have protective effects from some types of hearing loss. This study aimed to observe the protective effect of KRG in an ototoxic animal model using 3-NP intratympanic injection. BALB/c mice were classified into 5 groups (n =15) and dose-dependent toxic effects after intratympanic injection with 3-NP (300–5000mM) on the left ear were investigated to determine the appropriate toxicity level of 3-NP. For observation of the protective effects of KRG, 23 mice were grouped into 3-NP (500mM, n =12) and KRG+3-NP groups (300mg/kg KRG for 7 days before 500mM 3-NP administration, n =11). Auditory brain response (ABR) and cochlear morphological evaluations were performed before and after drug administration. The ABR thresholds in the 800–5000mM groups exceeded the maximum recording limit at 16 and 32kHz 1 day after 3-NP administration. The ABR threshold in the 500mM 3-NP+KRG group was significantly lower than that in the 500mM 3-NP group from post 1 week to 1 month. The mean type II fibrocyte counts significantly differed between the control and 3-NP groups and between the 3-NP and 3-NP+KRG groups. Spiral ganglion cell degeneration in the 3-NP group was more severe than that in the 3-NP+KRG group. This animal model exhibited a dose-dependent hearing loss with histological changes. KRG administration ameliorated the deterioration of hearing by 3-NP. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
0161813X
Volume :
34
Database :
Academic Search Index
Journal :
NeuroToxicology
Publication Type :
Academic Journal
Accession number :
85173554
Full Text :
https://doi.org/10.1016/j.neuro.2012.10.008