Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats.
Angiotensin-Converting Enzyme 2
/ genetics
Animals
Anti-Bacterial Agents
/ toxicity
Antihypertensive Agents
/ pharmacology
Auditory Threshold
/ drug effects
Cochlea
/ drug effects
Evoked Potentials, Auditory, Brain Stem
/ drug effects
Female
Heme Oxygenase (Decyclizing)
/ genetics
Kanamycin
/ toxicity
Ototoxicity
/ drug therapy
PPAR gamma
/ genetics
Rats
Rats, Sprague-Dawley
Telmisartan
/ pharmacology
aminoglycosides
angiotensin II receptor blocker
hearing loss
peroxisome proliferator activator receptor-γ
telmisartan
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
24 Nov 2021
24 Nov 2021
Historique:
received:
28
10
2021
revised:
23
11
2021
accepted:
23
11
2021
entrez:
10
12
2021
pubmed:
11
12
2021
medline:
18
12
2021
Statut:
epublish
Résumé
Telmisartan (TM) has been proposed to relieve inflammatory responses by modulating peroxisome proliferator activator receptor-γ (PPARγ) signaling. This study aimed to investigate the protective effects of TM on kanamycin(KM)-induced ototoxicity in rats. Forty-eight, 8-week-old female Sprague Dawley rats were divided into four groups: (1) control group, (2) TM group, (3) KM group, and (4) TM + KM group. Auditory brainstem response was measured. The histology of the cochlea was examined. The protein expression levels of angiotensin-converting enzyme 2 (ACE2), HO1, and PPARγ were measured by Western blotting. The auditory threshold shifts at 4, 8, 16, and 32 kHz were lower in the TM + KM group than in the KM group (all
Identifiants
pubmed: 34884516
pii: ijms222312716
doi: 10.3390/ijms222312716
pmc: PMC8657567
pii:
doi:
Substances chimiques
Anti-Bacterial Agents
0
Antihypertensive Agents
0
PPAR gamma
0
Kanamycin
59-01-8
Heme Oxygenase (Decyclizing)
EC 1.14.14.18
Hmox1 protein, rat
EC 1.14.14.18
Ace2 protein, rat
EC 3.4.17.23
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Telmisartan
U5SYW473RQ
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : NRF-2018R1D1A1B07048092
Organisme : National Research Foundation of Korea
ID : 2020R1A2C4002594
Organisme : Bundang CHA Medical Center
ID : RND2021-003
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