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神经性疼痛改变大鼠脊髓中的抗氧化活性。

Neuropathic pain modifies antioxidant activity in rat spinal cord.

作者信息

Guedes Renata P, Bosco Lidiane Dal, Teixeira Camila M, Araújo Alex S R, Llesuy Susana, Belló-Klein Adriane, Ribeiro Maria Flávia M, Partata Wania A

机构信息

Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, RS, Brasil.

出版信息

Neurochem Res. 2006 May;31(5):603-9. doi: 10.1007/s11064-006-9058-2. Epub 2006 May 23.

Abstract

Oxidative stress is an important pathophysiological mechanism of many neurological diseases. Reactive oxygen and nitrogen species have been cited as molecules involved in the nociceptive process. In this study, rats were submitted to sciatic nerve transection (SNT) for induction of neuropathic pain, and enzyme activities of SOD and catalase as well as lipid peroxidation (LPO) were measured in the lumbosacral spinal cord. The results show that LPO was not changed after SNT. SOD activity was reduced 7 days after SNT, while the change in catalase activity occurred on the third and seventh days in both sham and SNT animals. Hyperalgesia in SNT group was detected at the same points in time. These results suggest that SNT was not a strong enough stimulus to deplete all antioxidant content in the spinal cord, since increase in LPO was not detected. However, the role of oxidative stress in nociception can not be excluded.

摘要

氧化应激是许多神经疾病的重要病理生理机制。活性氧和氮被认为是参与伤害感受过程的分子。在本研究中,将大鼠进行坐骨神经横断术(SNT)以诱导神经性疼痛,并测量腰段脊髓中SOD和过氧化氢酶的酶活性以及脂质过氧化(LPO)。结果显示,SNT后LPO未发生变化。SNT后7天SOD活性降低,而在假手术组和SNT组动物中,过氧化氢酶活性在第3天和第7天均发生变化。在相同时间点检测到SNT组存在痛觉过敏。这些结果表明,SNT不是一个足够强烈的刺激来耗尽脊髓中的所有抗氧化剂含量,因为未检测到LPO增加。然而,氧化应激在伤害感受中的作用不能被排除。

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