Noise-induced hearing loss (NIHL) is the second most common cause of acquired hearing loss. Acoustic trauma can cause oxidative damage in the cochlear hair cells (HCs) through apoptotic pathways. Apelin is a newly discovered neuropeptide with neuroprotective effects against the oxidative stress in neurodegenerative disorder. We investigated the preventive effects of apelin-13 on the cochlear HCs and spiral ganglion neurons (SGNs) against acoustic trauma via Sirtuin-1 (Sirt-1) regulation in rats. Animals were assigned to control, control + apelin-13 (50 or 100 μg/kg, ip), and noise exposure groups without any treatment or were administered apelin-13 (50 or 100 μg/kg, ip) and EX-527 (an inhibitor of Sirt-1) prior to each noise session. In the noise groups, 110 dB white noise was applied for 6 h per 5 days. Pre- and post-exposure distortion product otoacoustic emissions (DPOAE) and cochlear superoxide dismutase (SOD) activity were assessed. Western blot evaluated the cochlear protein expressions of Sirt-1, cleaved-caspase-3, Bax, and Bcl-2. Cell apoptosis was detected through TUNEL staining. Immunofluorescence was used to examine expression of HCs and SGNs specific protein. DPOAE level were significantly improved in the noise exposure group receiving 100 μg/kg apelin-13. At high doses, apelin augmented SOD levels in the rat cochlea subjected to noise. Apelin 100 markedly increased Sirt-1, and decreased cleaved- caspase-3 expression as well as Bax/Bcl-2 ratio in the cochlea tissue of noise-exposed rats. These findings suggest the promising therapeutic potential of apelin-13 for the prevention of noise-induced injury to cochlea and hearing loss.

噪声性听力损失 (NIHL) 是获得性听力损失的第二大常见原因。声学创伤可通过凋亡途径导致耳蜗毛细胞 (HCs) 发生氧化损伤。Apelin 是一种新发现的神经肽，对神经退行性疾病中的氧化应激具有神经保护作用。我们通过 Sirtuin-1 (Sirt-1) 调节大鼠研究了 apelin-13 对耳蜗 HC 和螺旋神经节神经元 (SGN) 对听觉创伤的预防作用。动物被分配到对照组、对照组 + apelin-13 (50 或 100 μg/kg, ip) 和噪声暴露组，不进行任何治疗或给予 apelin-13 (50 或 100 μg/kg, ip) 和 EX-527 (在每次噪音会议之前，Sirt-1 的抑制剂。在噪声组中，每 5 天施加 110 dB 白噪声，持续 6 小时。评估了暴露前和暴露后畸变产物耳声发射 (DPOAE) 和耳蜗超氧化物歧化酶 (SOD) 活性。蛋白质印迹评估了 Sirt-1、cleaved-caspase-3、Bax 和 Bcl-2 的耳蜗蛋白表达。TUNEL染色检测细胞凋亡。免疫荧光用于检查 HCs 和 SGNs 特异性蛋白的表达。接受 100 μg/kg apelin-13 的噪声暴露组的 DPOAE 水平显着提高。在高剂量下，apelin 增加了受到噪音影响的大鼠耳蜗中的 SOD 水平。Apelin 100 在噪声暴露大鼠的耳蜗组织中显着增加了 Sirt-1，并降低了 cleaved-caspase-3 的表达以及 Bax/Bcl-2 的比率。这些发现表明，apelin-13 在预防噪音引起的耳蜗损伤和听力损失方面具有良好的治疗潜力。