朝鲜蓟叶水乙醇提取物可通过减轻坐骨神经氧化应激减轻慢性收缩损伤模型大鼠的神经痛。

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Mohammad Mehdi Haghighat Lari, Mohammad Reza Bakhoda, Mohammad Shabani, Mohsen Taghizadeh, Fereshteh Bahmani, Gholamali Hamidi, Fatemeh Aghighi, Sayyed Alireza Talaei
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引用次数: 0

摘要

神经病理性疼痛是神经损伤的一种后果,会出现感觉障碍、痛觉减退和异动症等症状。本研究旨在评估朝鲜蓟叶提取物对雄性大鼠坐骨神经慢性收缩性损伤(CCI)诱发的神经病理性疼痛的缓解潜力。大鼠以 200、400 和 800 毫克/千克的剂量灌胃服用朝鲜蓟叶水乙醇提取物 21 天。手术后第 1、4、7、14 和 21 天进行了行为测试。结果显示,只有 800 毫克/千克的剂量能显著减轻手术后第 14 天的热痛和异感,以及第 7 天的机械异感,其他剂量的剂量对行为没有影响。生化分析表明,朝鲜蓟提取物降低了坐骨神经组织中的脂质过氧化反应,并恢复了抗氧化酶(SOD和GPx)的活性。总之,服用朝鲜蓟叶提取物可提高大鼠坐骨神经的抗氧化能力并减少氧化应激,从而减轻神经病理性疼痛相关行为。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Artichoke leaf hydroethanolic extract reduces neuropathic pain in a rat model of chronic constriction injury via attenuating the sciatic nerve oxidative stress.

Neuropathic pain, a nerve damage consequence, presents symptoms such as dysesthesia, hyperalgesia, and allodynia. This study aimed to evaluate the alleviating potential of artichoke leaf extract in neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve in male rats. The hydroethanolic extract of artichoke leaf was administered via gavage at doses of 200, 400, and 800 mg/kg for 21 days. Behavioural tests were conducted on days 1, 4, 7, 14, and 21 post-surgeries. Only the dose of 800 mg/kg significantly reduced thermal hyperalgesia and allodynia from day 14 and mechanical allodynia from day 7, and the other doses did not affect behaviours. Biochemical analysis showed that artichoke extract decreased lipid peroxidation and restored antioxidant enzyme activities (SOD and GPx) in the sciatic nerve tissue. In conclusion, artichoke leaf extract administration diminishes neuropathic pain-related behaviours by enhancing antioxidant capacity and reducing oxidative stress in the rats' sciatic nerve.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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