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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >NADPH oxidase inhibitor apocynin decreases mitochondrial dysfunction and apoptosis in the ventral cochlear nucleus of D-galactose-induced aging model in rats
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NADPH oxidase inhibitor apocynin decreases mitochondrial dysfunction and apoptosis in the ventral cochlear nucleus of D-galactose-induced aging model in rats

机译：NADPH氧化酶抑制剂Apocynin降低了大鼠D-半乳糖诱导的老化模型的腹侧耳蜗核中的线粒体功能障碍和凋亡

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摘要

Presbycusis has become a common sensory deficit in humans. Oxidative damage to mitochondrial DNA and mitochondrial dysfunction is strongly associated with the aging of the auditory system. A previous study established a mimetic rat model of aging using D-galactose (D-gal) and first reported that NADPH oxidase-dependent mitochondria] oxidative damage and apoptosis in the ventral cochlear nucleus (VCN) might contribute to D-gal-induced central presbycusis. In this study, we investigated the effects of apocynin, an NADPH oxidase inhibitor, on mitochondrial dysfunction and mitochondria-dependent apoptosis in the VCN of D-gal-induced aging model in rats. Our data showed that apocynin decreased NADPH oxidase activity, H2O2 levels, mitochondrial DNA common deletion, and 8-hydroxy-2-deoxyguanosine (8-OHdG) expression and increased total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) activity in the VCN of D-gal-induced aging model in rats. Moreover, apocynin also decreased the protein levels of phospho-p47(phox)(p-p47(phox)), tumor necrosis factor alpha (TNF alpha), and uncoupling protein 2 (UCP2) in the VCN of D-gal-induced aging model in rats. Meanwhile, apocynin alleviated mitochondrial ultrastructure damage and enhanced ATP production and mitochondrial membrane potential (MMP) levels in the VCN of D-gal-induced aging model in rats. Furthermore, apocynin inhibited cytochrome c (Cyt c) translocation from mitochondria to the cytoplasm and suppressed caspase 3-dependent apoptosis in the VCN of D-gal-induced aging model in rats. Consequently, our findings suggest that neuronal survival promoted by an NADPH oxidase inhibitor is a potentially effective method to enhance the resistance of neurons to central presbycusis.
机译：Presbycusis已成为人类的常见感官赤字。对线粒体DNA和线粒体功能障碍的氧化损伤与听觉系统的老化强烈相关。先前的研究建立了使用D-半乳糖（D-GAL）的模拟大鼠老化模型，首先报道了腹侧耳蜗核（VCN）中的NADPH氧化酶依赖性线粒体。氧化损伤和凋亡可能有助于D-GAL诱导的中心presbycusis。在这项研究中，我们研究了NADPH氧化酶抑制剂在大鼠D-GAL诱导的老化模型VCN中的线粒体功能障碍和线粒体依赖性细胞凋亡的影响。我们的数据显示，呼吸蛋白蛋白氧化酶活性，H 2 O 2水平，线粒体DNA常见缺失和8-羟基-2-脱氧核苷酸（8-OHDG）表达和增加的总超氧化物歧化酶（T-SOD）和谷胱甘肽过氧化物酶（GSH-PX）大鼠D-GAL诱导老化模型VCN的活性。此外，Apocynin还降低了D-Gal诱导的老化VCN中的磷酸-P47（PHOX）（P-P47（PHOX）），肿瘤坏死因子α（TNFα）和解偶联蛋白2（UCP2）的蛋白质水平大鼠模型。同时，呼吸突染症在大鼠D-GAL诱导的老化模型VCN中缓解了线粒体超微结构损伤和增强的ATP生产和线粒体膜电位（MMP）水平。此外，呼吸蛋白蛋白抑制来自线粒体的细胞色素C（cyt c）易位，在大鼠D-GAL诱导的衰老模型VCN中抑制了Caspase 3依赖性凋亡。因此，我们的研究结果表明，NADPH氧化酶抑制剂促进的神经元存活是一种增强神经元对中央预平血清的抗性的潜在有效的方法。

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