Lee Yeong Ro, Hong Bin Na, Her You Ri, Castañeda Rodrigo, Moon Hyo Won, Kang Tong Ho
Graduate School of Biotechnology, Kyung Hee University, Global Campus, Gyeonggi 446-701, Republic of Korea ; Department of Oriental Medicinal Materials & Processing, College of Life Sciences, Kyung Hee University, Global Campus, Gyeonggi 446-701, Republic of Korea.
Department of Oriental Medicinal Materials & Processing, College of Life Sciences, Kyung Hee University, Global Campus, Gyeonggi 446-701, Republic of Korea ; Department of Audiology, Nambu University, Gwangju 506-824, Republic of Korea.
Evid Based Complement Alternat Med. 2015;2015:230747. doi: 10.1155/2015/230747. Epub 2015 Mar 24.
Diabetes mellitus (DM) is a metabolic disease that involves disorders such as diabetic retinopathy, diabetic neuropathy, and diabetic hearing loss. Recently, neurotrophin has become a treatment target that has shown to be an attractive alternative in recovering auditory function altered by DM. The aim of this study was to evaluate the effect of DA9801, a mixture of Dioscorea nipponica and Dioscorea japonica extracts, in the auditory function damage produced in a STZ-induced diabetic model and to provide evidence of the mechanisms involved in enhancing these protective effects. We found a potential application of DA9801 on hearing impairment in the STZ-induced diabetic model, demonstrated by reducing the deterioration produced by DM in ABR threshold in response to clicks and normalizing wave I-IV latencies and Pa latencies in AMLR. We also show evidence that these effects might be elicited by inducing NGF related through Nr3c1 and Akt. Therefore, this result suggests that the neuroprotective effects of DA9801 on the auditory damage produced by DM may be affected by NGF increase resulting from Nr3c1 via Akt transformation.
糖尿病(DM)是一种代谢性疾病,涉及糖尿病视网膜病变、糖尿病神经病变和糖尿病听力损失等病症。最近,神经营养因子已成为一种治疗靶点,在恢复因糖尿病改变的听觉功能方面显示出是一种有吸引力的替代方法。本研究的目的是评估穿龙薯蓣和日本薯蓣提取物的混合物DA9801对链脲佐菌素诱导的糖尿病模型中产生的听觉功能损伤的影响,并为增强这些保护作用所涉及的机制提供证据。我们发现DA9801在链脲佐菌素诱导的糖尿病模型中对听力损伤有潜在应用,这通过降低糖尿病引起的听性脑干反应(ABR)阈值对短声的恶化以及使听性中潜伏期反应(AMLR)中的I-IV波潜伏期和Pa潜伏期正常化得以证明。我们还表明,这些作用可能是通过诱导经由Nr3c1和Akt相关的神经生长因子(NGF)而引发的。因此,该结果表明,DA9801对糖尿病所致听觉损伤的神经保护作用可能受Nr3c1经Akt转化导致的NGF增加的影响。