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RISS 인기검색어
- 검색키워드
- 저자 : 알폰스 우무기레 (검색결과 1 건)
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Protective Effect of Avenanthramide-C on Ototoxicity
Introduction: There are many types of hearing loss and sensorineural hearing loss ranks among them. However, no adequate treatment has so far been elucidated to rectify this problem. Noise exposure causes various physical damages and major cellular changes within the cochlea systems that result in hearing loss, with outer hair cells (OHCs) located at the basal turn of the cochlea being most vulnerable and susceptible pathological targets and lost in first instance. Reactive Oxygen Species (ROS) found in the cochlea orchestrates cascade reactions with different molecules within the cochlea and disrupt normal physiological mechanisms, and results in hair cell death and lesion with permanent hearing loss as an endpoint. Avenanthramides (AVNs) extracted from oats possess antioxidant properties to reduce free radicals, and exert adequate protection on various cell types. In this present study, I wanted to investigate whether AVN-C can protect auditory hair cell and preserve hearing from ototoxicity. Methods: B6 mouse was randomly used in 6 to 12 subjects per individual study group. Mouse tissue fluid samples were analyzed using Liquid Chromatography-mass spectrophotometry (LM/MS), to detect AVN-C into mouse tissue fluids. Animals were subjected to noise stimuli centered at 95 and 100 dB, 8 kHz for 6 hours once a day for various length of time with or without pre-treatment of 10 mg/Kg of AVN-C. Click and frequency stimuli were determined in a decreasing order from 90 to 10 dB of visual auditory brainstem response (ABR) threshold. OHCs were visualized by immunohistochemistry using confocal microscope. HEI-OC cells were cultured under normal and standard conditions, treated with AVN-C 5 hours following the culture. Gentamicin was added to the HEI-OC cell media culture 24 hours later, to generate cell ototoxicity in vitro. Flow cytometry and real-time quantitative polymerase chain reaction (RT-qPCR) were conducted and results analyzed. Statistical significance was determined using SPSS 17.0 (SPSS Inc., Chicago, IL, USA), independent student t-test was used for pairs of data with significance set at p<0.05. Results: AVN-C reached its climax into mouse serum after 1 hour post intraperitoneal administration and decreased with time, to be washed out within 6 hours. Furthermore, AVN-C crossed blood brain barrier and peaked within 2 hours. The permeability of AVN-C towards blood labyrinth barrier was outlined by its presence into perilymph and noise exposure enhanced its clearance. Both noise stimuli centered at 95 and 100 dB respectively, were responsible to cause hearing loss at 1 week post exposure; with a complete recovery observed with time. Pre-treatment of AVN-C 24 hours contributed to preserve hearing vis-à-vis to noise exposure, moreover subjects regained their threshold shifts at their baseline implying temporary threshold shift. Overstimulation with 100 dB for 7 days consecutively triggered significant impact of threshold shift in exposed subjects, however 30 minutes pre-administration of 10 mg/Kg of AVN-C to subjects at each noise time point, proved to procure prominent protection to noise exposed subjects, one month post noise exposure. Cochlea histological analysis demonstrated loss of OHCs at the basal turn in noise induced only group, and preservation of OHCs in AVN-C pre-treated subjects confirming the noteworthy protective effect provided by AVN-C over noise overexposure. AVN-C exhibited protective effect, and thwarted the toxicity caused by gentamicin when treated to HEI-OC cell culture 24 hours in advance to Gentamicin. Several apoptotic and ROS genes were down-regulated by AVN-C. Conclusion: AVN-C provided a protective effect over ototoxicity in noise overexposed subjects, and revealed to be a good candidate molecule for future preventive therapy on ototoxic sensorineural hearing loss.
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