烟酰胺腺嘌呤二核苷酸
螺旋神经节
体内
离体
内耳
药理学
NAD+激酶
听力损失
药物输送
细胞生物学
化学
医学
生物医学工程
体外
生物化学
材料科学
解剖
纳米技术
生物
酶
听力学
生物技术
作者
Baoyi Feng,Tingting Dong,Xinyu Song,Xiaofei Zheng,Chenxi Jin,Zhenzhe Cheng,Yiqing Liu,Wenjie Zhang,Xueling Wang,Yong Tao,Hao Wu
标识
DOI:10.1002/advs.202305682
摘要
Abstract There are no Food and Drug Administration‐approved drugs for treating noise‐induced hearing loss (NIHL), reflecting the absence of clear specific therapeutic targets and effective delivery strategies. Noise trauma is demonstrated results in nicotinamide adenine dinucleotide (NAD+) downregulation and mitochondrial dysfunction in cochlear hair cells (HCs) and spiral ganglion neurons (SGNs) in mice, and NAD+ boosted by nicotinamide (NAM) supplementation maintains cochlear mitochondrial homeostasis and prevents neuroexcitatory toxic injury in vitro and ex vivo, also significantly ameliorated NIHL in vivo. To tackle the limited drug delivery efficiency due to sophisticated anatomical barriers and unique clearance pathway in ear, personalized NAM‐encapsulated porous gelatin methacryloyl (PGMA@NAM) are developed based on anatomy topography of murine temporal bone by micro‐computed tomography and reconstruction of round window (RW) niche, realizing hydrogel in situ implantation completely, NAM sustained‐release and long‐term auditory preservation in mice. This study strongly supports personalized PGMA@NAM as NIHL protection drug with effective inner ear delivery, providing new inspiration for drug‐based treatment of NIHL.
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