Hyperbaric Oxygen Treatment Improves Hearing Level Attenuating TLR4/NF-κB Mediated Inflammation in Sudden Sensorineural Hearing Loss Patients.
- Author:
Xue Hua LIU
1
;
Fang LIANG
1
;
Xing Yuan JIA
2
;
Lin ZHAO
3
;
Yan ZHOU
2
;
Jing YANG
1
Author Information
- Publication Type:Journal Article
- Keywords: Hyperbaric oxygen treatment; Nuclear factor-kB; Sudden sensorineural hearing loss; Toll-like receptor 4
- MeSH: Adolescent; Adult; Aged; China; Female; Hearing Loss, Sensorineural; therapy; Hearing Loss, Sudden; therapy; Humans; Hyperbaric Oxygenation; Inflammation; genetics; therapy; Male; Middle Aged; NF-kappa B p50 Subunit; genetics; metabolism; Toll-Like Receptor 4; genetics; metabolism; Young Adult
- From: Biomedical and Environmental Sciences 2020;33(5):331-337
- CountryChina
- Language:English
-
Abstract:
Objective:Hyperbaric oxygen treatment (HBOT) has demonstrated efficacy in improving hearing levels of patients with idiopathic sudden sensorineural hearing loss (ISSHL); however, the underlying mechanisms are not well understood. HBOT alleviates the inflammatory response, which is mediated by Toll-like receptor (TLR) 4 and nuclear factor (NF)-κB. In this study we investigated whether HBOT attenuates inflammation in ISHHL patients alteration of TLR4 and NF-κB expression.
Methods:ISHHL patients ( = 120) and healthy control subjects ( = 20) were enrolled in this study. Patients were randomly divided into medicine group treated with medicine only ( = 60) and HBO group receiving both HBOT and medicine ( = 60). Audiometric testing was performed pre- and post-treatment. TLR4, NF-кB, and TNF-α expression in peripheral blood of ISSHL patients and healthy control subjects was assessed by ELISA before and after treatment.
Results:TLR4, NF-κB, and TNF-α levels were upregulated in ISSHL patients relative to healthy control subjects; the levels were decreased following treatment and were lower in the HBO group than that in the medicine group post-treatment ( < 0.05 and < 0.01).
Conclusion:HBOT alleviates hearing loss in ISSHL patients by suppressing the inflammatory response induced by TLR4 and NF-κB signaling.