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首页> 外文期刊>Toxicology and Applied Pharmacology >Carvedilol prevents functional deficits in peripheral nerve mitochondria of rats with oxaliplatin-evoked painful peripheral neuropathy
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Carvedilol prevents functional deficits in peripheral nerve mitochondria of rats with oxaliplatin-evoked painful peripheral neuropathy

机译：Carvedilol通过Oxaliplatin诱发的痛苦周围神经病变，防止大鼠外周神经线粒体中的功能缺陷

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Oxaliplatin use as chemotherapeutic agent is frequently limited by cumulative neurotoxicity which may compromise quality of life. Reports relate this neurotoxic effect to oxidative stress and mitochondrial dysfunction in peripheral nerves and dorsal root ganglion (DRG). Carvedilol is an antihypertensive drug, has also been appreciated for its antioxidant and mitoprotective properties. Carvedilol co-treatment did not reduce the anti-tumor effects of oxaliplatin in human colon cancer cells (HT-29), but exhibited free radical scavenging activity against oxaliplatin-induced oxidative stress in neuronal cells (Neuro-2a). Hence, the present study was designed to investigate the effect of carvedilol in the experimental model of oxaliplatin-induced peripheral neuropathy (OIPN) in Sprague-Dawley rats. Oxaliplatin reduced the sensory nerve conduction velocity and produced the thermal and mechanical nociception. Carvedilol significantly (P < 0.001) attenuated these functional and sensorimotor deficits. It also counteracted oxidative/nitrosative stress by reducing the levels of nitrotyrosine and improving the mitochondrial superoxide dismutase expression in both sciatic nerve and DRG tissues. It improved the mitochondria] function and prevented the oxaliplatin-induced alteration in mitochondrial membrane potential in sciatic nerve thus prevented loss of intra epidermal nerve fiber density in the foot pads. Together the results prompt the use of carvedilol along with chemotherapy with oxaliplatin to prevent the peripheral neuropathy. (C) 2017 Elsevier Inc. All rights reserved.
机译：奥沙利铂作为化疗药物的使用经常受到累积神经毒性的限制，这可能会影响生活质量。有报道称，这种神经毒性作用与外周神经和背根神经节（DRG）的氧化应激和线粒体功能障碍有关。卡维地洛是一种抗高血压药物，也因其抗氧化和保护作用而受到重视。卡维地洛联合治疗不会降低奥沙利铂对人结肠癌细胞（HT-29）的抗肿瘤作用，但对奥沙利铂诱导的神经细胞氧化应激（Neuro-2a）表现出自由基清除活性。因此，本研究旨在研究卡维地洛在Sprague-Dawley大鼠奥沙利铂诱导的周围神经病变（OIPN）实验模型中的作用。奥沙利铂降低感觉神经传导速度，产生热伤害和机械伤害。卡维地洛显著（P<0.001）减轻了这些功能和感觉运动缺陷。它还通过降低硝基酪氨酸水平和改善坐骨神经和DRG组织中线粒体超氧化物歧化酶的表达来对抗氧化/亚硝化应激。它改善了线粒体的功能，防止了奥沙利铂诱导的坐骨神经线粒体膜电位的改变，从而防止了脚垫表皮内神经纤维密度的丢失。这些结果促使卡维地洛与奥沙利铂联合化疗预防周围神经病变。（C） 2017爱思唯尔公司版权所有。

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