Protective Effect of Yang Mi Ryung® Extract on Noise-Induced Hearing Loss in Mice

Noise-induced hearing loss (NIHL) results from the damage of the delicate hair cells inside the ear after excessive stimulation of noise. Unlike certain lower animals such as amphibians, fishes, and birds, in humans, hair cells cannot be regenerated once they are killed or damaged; thus, there are no therapeutic options to cure NIHL. Therefore, it is more important to protect hair cells from the noise before the damage occurs. In this study, we report the protective effect of Yang Mi Ryung extract (YMRE) against NIHL; this novel therapeutic property of YMRE has not been reported previously. Our data demonstrates that the hearing ability damaged by noise is markedly restored in mice preadministrated with YMRE before noise exposure, to the level of normal control group. Our study also provides the molecular mechanism underlying the protective effect of YMRE against NIHL by showing that YMRE significantly blocks noise-induced apoptotic cell death and reduces reactive oxygen species (ROS) production in cochleae. Moreover, quantitative polymerase chain reaction (qPCR) analysis demonstrates that YMRE has anti-inflammatory properties, suppressing the mRNA levels of TNFα and IL-1β induced by noise exposure. In conclusion, YMRE could be a useful preventive intervention to prevent hearing impairment induced by the exposure to excessive noise.

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Effect of Phlorofucofuroeckol A and Dieckol Extracted from Ecklonia cava on Noise-induced Hearing Loss in a Mouse Model

Marine Drugs ◽

10.3390/md19080443 ◽

2021 ◽

Vol 19 (8) ◽

pp. 443

Author(s):

Hyunjun Woo ◽

Min-Kyung Kim ◽

Sohyeon Park ◽

Seung-Hee Han ◽

Hyeon-Cheol Shin ◽

...

Keyword(s):

Hearing Loss ◽

Hair Cell ◽

Noise Exposure ◽

Radical Scavenging ◽

Threshold Shift ◽

Ecklonia Cava ◽

Control Group ◽

Noise Induced Hearing Loss ◽

Antioxidant Agents ◽

Brainstem Response

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.

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Associations of Genetic Variation in Glyceraldehyde 3-Phosphate Dehydrogenase Gene with Noise-Induced Hearing Loss in a Chinese Population: A Case-Control Study

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph17082899 ◽

2020 ◽

Vol 17 (8) ◽

pp. 2899 ◽

Cited By ~ 1

Author(s):

Liu Wan ◽

Boshen Wang ◽

Juan Zhang ◽

Baoli Zhu ◽

Yuepu Pu

Keyword(s):

Hearing Loss ◽

Genetic Variation ◽

Chinese Population ◽

Case Control Study ◽

Quantitative Polymerase Chain Reaction ◽

Case Control ◽

Control Group ◽

Case Group ◽

Noise Induced Hearing Loss ◽

Control Study

Objective: The purpose of this paper was to clarify the association between genetic variation in the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene and the risk of noise-induced hearing loss (NIHL). Methods: A case-control study (633 cases and 625 controls) was conducted in this study. Logistic regression was used to analyze the relationships between environmental and individual factors and NIHL. Gene expression levels were compared among each GAPDH rs6489721 genotype and between the case and control groups based on real-time fluorescence quantitative Polymerase Chain Reaction (PCR). Results: The T allele of GADPH rs6489721 was significantly associated with NIHL (odds ratio (OR) = 1.262, 95% confidence interval (CI) (1.066, 1.493), p = 0.006) and showed strong associations in the codominant and dominant models (TT vs. CC: OR = 1.586, 95% CI (1.131, 2.225), p = 0.008; TT vs. TC/CC: OR = 1.391, 95% CI (1.073, 1.804), p = 0.013). The expression level of the TT genotype was significantly higher than that of the CC genotype (p = 0.012), and the expression of the case group was also higher than that of the control group (p = 0.013). Conclusions: The homozygous risk allele (TT) of rs6489721 was associated with an enhanced GAPDH expression, resulting in the development of NIHL in a Chinese population.

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Treatment With Calcineurin Inhibitor FK506 Attenuates Noise-Induced Hearing Loss

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.648461 ◽

2021 ◽

Vol 9 ◽

Author(s):

Zu-Hong He ◽

Song Pan ◽

Hong-Wei Zheng ◽

Qiao-Jun Fang ◽

Kayla Hill ◽

...

Keyword(s):

Hearing Loss ◽

Hair Cells ◽

Calcineurin Inhibitor ◽

Noise Exposure ◽

Cell Loss ◽

Outer Hair Cells ◽

Oxygen Species ◽

Noise Induced Hearing Loss ◽

Activated T Cells ◽

Interfering Rna

Attenuation of noise-induced hair cell loss and noise-induced hearing loss (NIHL) by treatment with FK506 (tacrolimus), a calcineurin (CaN/PP2B) inhibitor used clinically as an immunosuppressant, has been previously reported, but the downstream mechanisms of FK506-attenuated NIHL remain unknown. Here we showed that CaN immunolabeling in outer hair cells (OHCs) and nuclear factor of activated T-cells isoform c4 (NFATc4/NFAT3) in OHC nuclei are significantly increased after moderate noise exposure in adult CBA/J mice. Consequently, treatment with FK506 significantly reduces moderate-noise-induced loss of OHCs and NIHL. Furthermore, induction of reactive oxygen species (ROS) by moderate noise was significantly diminished by treatment with FK506. In agreement with our previous finding that autophagy marker microtubule-associated protein light chain 3B (LC3B) does not change in OHCs under conditions of moderate-noise-induced permanent threshold shifts, treatment with FK506 increases LC3B immunolabeling in OHCs after exposure to moderate noise. Additionally, prevention of NIHL by treatment with FK506 was partially abolished by pretreatment with LC3B small interfering RNA. Taken together, these results indicate that attenuation of moderate-noise-induced OHC loss and hearing loss by FK506 treatment occurs not only via inhibition of CaN activity but also through inhibition of ROS and activation of autophagy.

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Effects of D-methionine in mice with noise-induced hearing loss mice

Journal of International Medical Research ◽

10.1177/0300060519860679 ◽

2019 ◽

Vol 47 (8) ◽

pp. 3874-3885 ◽

Cited By ~ 2

Author(s):

Yanru Wang ◽

Yan Qu ◽

Xuzhen Chen ◽

Pu Zhang ◽

Dan Su ◽

...

Keyword(s):

Hearing Loss ◽

Basement Membrane ◽

Mouse Model ◽

Hair Cells ◽

Noise Exposure ◽

Stria Vascularis ◽

Connexin 26 ◽

Noise Induced Hearing Loss ◽

Expression Levels ◽

Brainstem Response

Objective To study the effects of D-methionine in a mouse model of noise-induced hearing loss (NIHL). Methods We investigated changes in auditory function and microscopic cochlear structure in a mouse model of NIHL, and carried out 4-hydroxynonenal (4-HNE) immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labeling, and examined expression levels of connexins 26 and 30 by western blot. Results The auditory brainstem response threshold was significantly increased by noise exposure. Noise exposure also damaged the inner and particularly the outer hair cells in the cochlear basement membrane, while histochemistry demonstrated only scattered loss of hair cells in the basement membrane in mice treated with D-methionine before or after noise exposure. D-methionine inhibited apoptosis in the cochlear basement membrane, stria vascularis, and spiral ligament. 4-HNE expression in the basement membrane, stria vascularis, and spiral collateral ligament was increased by noise exposure, but this increase was attenuated by D-methionine. Connexin 26 and connexin 30 expression levels were reduced by noise exposure, and this effect was similarly attenuated by D-methionine administered either before or after noise exposure. Conclusion D-methionine administered before or after noise exposure could rescue NIHL by protecting cochlear morphology, inhibiting apoptosis, and maintaining connexin 26 and 30 expression.

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Research and Discussion on the Relationships between Noise-Induced Hearing Loss and ATP2B2 Gene Polymorphism

International Journal of Genomics ◽

10.1155/2019/5048943 ◽

2019 ◽

Vol 2019 ◽

pp. 1-8

Author(s):

Suhao Zhang ◽

Enmin Ding ◽

Haoyang Yin ◽

Hengdong Zhang ◽

Baoli Zhu

Keyword(s):

Hearing Loss ◽

Gene Polymorphism ◽

Noise Exposure ◽

Venous Blood ◽

Pure Tone Audiometry ◽

Control Group ◽

Case Group ◽

Noise Induced Hearing Loss ◽

Cochlear Hair Cells ◽

Potential Biomarker

Long-term and continuous noise exposure can result in noise-induced hearing loss (NIHL), which is a worldwide problem resulting from the interaction of environmental and genetic factors. The ATP2B2 gene polymorphism can destroy cochlear hair cells and increase the risk of NIHL. A case-control study of 760 Chinese textile workers was conducted to investigate the relationship between ATP2B2 polymorphisms and NIHL susceptibility. Venous blood was collected and questionnaires were conducted by professional physicians. A case group and a control group which were typed by individuals’ pure-tone audiometry test results were set. Three polymorphism sites of ATP2B2 were genotyped by using the PCR technique. Analysis results revealed that the C allele of rs3209637 (95%CI=1.08–2.58, odds ratio OR=1.67, P=0.027) was a dangerous factor and could add to risks of NIHL in the Chinese employees. The data of stratified analysis revealed that individuals who are exposed to noise>95 dB with the rs3209637 C genotype have a higher susceptibility to NIHL (OR=1.34, 95%CI=1.07–1.68). Multifactor dimensionality reduction analysis revealed that the interaction between rs14154 and rs3209637 is linked to increased NIHL risk, and for the interaction among rs14154, smoking and drinking had the same function (OR=1.54 and 1.77, 95%CI=1.15–2.07, 1.33–2.37, and P=0.0037 and P<0.0001, respectively). Our results suggest that genetic polymorphism rs3209637 C within ATP2B2 is a risk factor for NIHL among Chinese employees and rs3209637 C could be a potential biomarker for NIHL patients.

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Relationship between CDH23 gene and risk of noise-induced hearing loss

10.21203/rs.3.rs-276861/v1 ◽

2021 ◽

Author(s):

Jie Jiao ◽

Shanfa Yu ◽

Guizhen Gu ◽

Guoshun Chen ◽

Huanling Zhang ◽

...

Keyword(s):

Hearing Loss ◽

Noise Exposure ◽

Control Group ◽

Case Group ◽

Noise Induced Hearing Loss ◽

Nucleotide Polymorphisms ◽

Significant Relationships ◽

Increased Risk ◽

Main Effects ◽

The Relationship

Abstract Objective: To investigate the relationship between CDH23 gene and the risk of noise-induced hearing loss (NIHL).Methods: This was a case-control study. Noise-exposed workers worked in a steel factory in North China was recruited and been divided into two groups: the case group (BHFTA ≥40 dB) and the control group (BHFTA<25 dB). We analyzed the association among 18 single nucleotide polymorphisms (SNPs) in CDH23 and NIHL risk using the generalized multifactor dimensionality reduction (GMDR) method. Logistic regression was performed to analyze the main effects of SNPs and the interactions between CNE and SNPs adjusting cumulative noise exposure (CNE), smoking, drinking, physical exercise and hypertension. Results: In this study, 776 subjects of period I and 1117 subjects of period I+II were recruited. The results showed that subjects who carried the AA genotype of rs3802711possessed significantly increased risk of NIHL than those carrying GG (OR: 2.71; 95% CI:1.15, 6.39) and GA+GG (OR: 2.54; 95% CI: 1.09, 6.00) in period I, respectively. For rs11592462, subjects carrying the GG genotype showed a significantly increased risk of NIHL compared with the subjects. Significant relationships were showed between rs10999947, rs3802711, rs10762480, rs3752751, rs3752752, rs3747867, and rs11592462 for NIHL overall and various CNE strata. There was no significant association between the rs1227049 - rs3752752 - rs10999947 - rs3752751 - rs10762480 - rs3802711 - rs11592462 - rs4747195 - rs4747194 - rs10466026 haplotypes and NIHL risk. Conclusions: The genetic variation in the CDH23 gene might play an important role in determining individual susceptibility to NIHL.

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Inhibition of Cochlear HMGB1 Expression Attenuates Oxidative Stress and Inflammation in an Experimental Murine Model of Noise-Induced Hearing Loss

Cells ◽

10.3390/cells10040810 ◽

2021 ◽

Vol 10 (4) ◽

pp. 810

Author(s):

Cheng-Ping Shih ◽

Chao-Yin Kuo ◽

Yuan-Yung Lin ◽

Yi-Chun Lin ◽

Hang-Kang Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Hearing Loss ◽

Noise Exposure ◽

Outer Hair Cells ◽

Control Group ◽

Noise Induced Hearing Loss ◽

Post Exposure ◽

Nadph Oxidase 4 ◽

Brainstem Response ◽

Ros Formation

Noise-induced hearing loss (NIHL) is a common inner ear disease but has complex pathological mechanisms, one of which is increased oxidative stress in the cochlea. The high-mobility group box 1 (HMGB1) protein acts as an inflammatory mediator and shows different activities with redox modifications linked to the generation of reactive oxygen species (ROS). We aimed to investigate whether manipulation of cochlear HMGB1 during noise exposure could prevent noise-induced oxidative stress and hearing loss. Sixty CBA/CaJ mice were divided into two groups. An intraperitoneal injection of anti-HMGB1 antibodies was administered to the experimental group; the control group was injected with saline. Thirty minutes later, all mice were subjected to white noise exposure. Subsequent cochlear damage, including auditory threshold shifts, hair cell loss, expression of cochlear HMGB1, and free radical activity, was then evaluated. The levels of HMGB1 and 4-hydroxynonenal (4-HNE), as respective markers of reactive nitrogen species (RNS) and ROS formation, showed slight increases on post-exposure day 1 and achieved their highest levels on post-exposure day 4. After noise exposure, the antibody-treated mice showed markedly less ROS formation and lower expression of NADPH oxidase 4 (NOX4), nitrotyrosine, inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM‑1) than the saline-treated control mice. A significant amelioration was also observed in the threshold shifts of the auditory brainstem response and the loss of outer hair cells in the antibody-treated versus the saline-treated mice. Our results suggest that inhibition of HMGB1 by neutralization with anti-HMGB1 antibodies prior to noise exposure effectively attenuated oxidative stress and subsequent inflammation. This procedure could therefore have potential as a therapy for NIHL.

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Plasma Metabolomic Profiling in Workers With Noise-induced Hearing Loss: A Pilot Study

10.21203/rs.3.rs-437429/v1 ◽

2021 ◽

Author(s):

Long Miao ◽

Boshen Wang ◽

Juan Zhang ◽

Lihong Yin ◽

Yuepu Pu

Keyword(s):

Hearing Loss ◽

Acid Metabolism ◽

White Blood Cells ◽

Partial Least Square ◽

Plasma Metabolites ◽

Control Group ◽

Mrna Levels ◽

Noise Induced Hearing Loss ◽

Autophagy Pathway ◽

Potential Biomarkers

Abstract Noise-induced hearing loss (NIHL) remains a leading occupational related disease and is a serious public health problem. Hence, the identification of potential biomarkers for NIHL prevention and diagnosis has become an urgent work. To discover potential metabolic biomarkers of NIHL, plasma metabolomics analysis among 62 NIHL patients and 62 controls was performed using ultrahigh performance liquid chromatography-mass spectrometry (UPLC/MS). Orthogonal partial least square-discriminant analysis (OPLS-DA) model was applied to distinguish metabolite profile alterations in plasma samples between the two groups. The alterations in autophagy pathway were in accordance with previous published studies, therefore, three autophagy-related genes (PI3K, AKT and ATG5) were selected and mRNA levels were detected by RT-qPCR analysis in peripheral white blood cells (WBCs) samples. Compared to the control group, 20 identified plasma metabolites were significantly altered in NIHL patients. Meanwhile, a total of seven metabolic pathways were enriched, including glycerophospholipid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, autophagy, choline metabolism, alpha-linolenic acid metabolism and linoleic acid metabolism, and retrograde endocannabinoid signaling pathway. Furthermore, the results indicated that the mRNA levels of three autophagy-related genes (PI3K, AKT and ATG5) were significantly decreased in NIHL cases compared with controls. Taken together, our current study firstly provides evidence that the identified aberrantly altered metabolites might be potential biomarkers of NIHL for noise-exposed workers. In addition, autophagy pathway may be involved in the occurrence and development of NIHL.

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Effect of Electroacupuncture on Noise-Induced Hearing Loss in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/9114676 ◽

2021 ◽

Vol 2021 ◽

pp. 1-8

Author(s):

Chia-Hao Chang ◽

Chia-Der Lin ◽

Ching-Liang Hsieh

Keyword(s):

Hearing Loss ◽

Noise Exposure ◽

Histopathological Examination ◽

Spiral Ganglion ◽

Auditory Brainstem ◽

Auditory Threshold ◽

Auditory Brainstem Responses ◽

Control Group ◽

Noise Induced Hearing Loss ◽

Ganglion Neurons

Acupuncture has long been used to relieve some inner ear diseases such as deafness and tinnitus. The present study examined the effect of electroacupuncture (EA) on noise-induced hearing loss (NIHL) in animals. A NIHL rat model was established. Electroacupuncture pretreatment at 2 Hz or posttreatment at the right Zhongzhu (TE3) acupoint was applied for 1 hour. Auditory thresholds were measured using auditory brainstem responses (ABRs), and histopathology of the cochlea was examined. The results indicated that the baseline auditory threshold of ABR was not significantly different between the control (no noise), EA-only (only EA without noise), noise (noise exposure only), pre-EA (pretreating EA then noise), and post-EA (noise exposure then posttreating with EA) groups. Significant auditory threshold shifts were found in the noise, pre-EA, and post-EA groups in the immediate period after noise exposure, whereas auditory recovery was better in the pre-EA and post-EA groups than that in the noise group at the three days, one week (W1), two weeks (W2), three weeks (W3), and four weeks(W4) after noise stimulation. Histopathological examination revealed greater loss of the density of spiral ganglion neurons in the noise group than in the control group at W1 and W2. Although significant loss of spiral ganglion loss happened in pre-EA and post-EA groups, such loss was less than the loss of the noise group, especially W1. These results indicate that either pretreatment or posttreatment with EA may facilitate auditory recovery after NIHL. The detailed mechanism through which EA alleviates NIHL requires further study.

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A systematic review of the interventions to promote the wearing of hearing protection

Sao Paulo Medical Journal ◽

10.1590/s1516-31802007000600013 ◽

2007 ◽

Vol 125 (6) ◽

pp. 362-369 ◽

Cited By ~ 10

Author(s):

Regina Paolucci El Dib ◽

Álvaro Nagib Atallah ◽

Régis Bruni Andriolo ◽

Bernardo Garcia de Oliveira Soares ◽

Jos Verbeek

Keyword(s):

Hearing Loss ◽

Noise Exposure ◽

Controlled Trial ◽

Intervention Group ◽

General Information ◽

Control Group ◽

Hearing Protection ◽

Noise Induced Hearing Loss ◽

School Based ◽

Source Studies

CONTEXT AND OBJECTIVE: Noise-induced hearing loss can only be prevented by eliminating or lowering noise exposure levels. When the source of the noise cannot be eliminated, workers have to rely on hearing protection equipment. The aim here was to summarize the evidence for the effectiveness of interventions to enhance the wearing of hearing protection among workers exposed to noise in the workplace. DATA SOURCE: Studies with random assignment were identified by an electronic search of the medical literature up to 2005. Data were double-entered into the Review Manager software, version 4.2.5. DATA SYNTHESIS: Two studies were found. A computer-based intervention tailored to individual workers’ risks and lasting 30 minutes was not found to be more effective than a video providing general information for workers. A second randomized controlled trial evaluated the effect of a four-year school-based hearing loss prevention program among schoolchildren working on their parents’ farms. The intervention group was twice as likely to wear some kind of hearing protection as was the control group (which received only minimal intervention). REVIEWERS’ CONCLUSIONS: The limited evidence does not show whether tailored interventions are more or less effective than general interventions among workers, 80% of whom already use hearing protection. Long-lasting school-based interventions may increase the use of hearing protection substantially. Better interventions to enhance the use of hearing protection need to be developed and evaluated in order to increase the prevention of noise-induced hearing loss among workers.

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