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没食子酸对紫杉醇诱导的小鼠神经性疼痛的改善作用。

Ameliorative effect of gallic acid in paclitaxel-induced neuropathic pain in mice.

作者信息

Kaur Satbir, Muthuraman Arunachalam

机构信息

Department of Pharmacology, Chaudhary Devi Lal College of Pharmacy, BD Sharma University of Health Science, Yamuna Nagar, Yamuna Nagar-135003, Haryana, India.

Department of Pharmacology and Toxicology, Akal College of Pharmacy & Technical Education, Punjab Technical University (Jalandhar), Mastuana Sahib, Sangrur-147001, Punjab, India.

出版信息

Toxicol Rep. 2019 Jun 7;6:505-513. doi: 10.1016/j.toxrep.2019.06.001. eCollection 2019.

Abstract

The present study has been investigated the role of gallic acid (GA) in paclitaxel-induced neuropathic pain. The neuropathic pain was developed with paclitaxel (PT: 2 mg/kg, ) administration in mice. GA (20 and 40 mg/kg) and pregabalin (PreG: 5 mg/kg) were administered intravenously for 10 consecutive days. The neuralgic sensations were investigated by assessing various pain tests like acetone drop, pinprick, plantar, tail flick, and tail pinch test. Mice pain behaviors were evaluated on 0, 4, 8, 12 and 16 days. The levels of sciatic nerve thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide anion, calcium, myeloperoxidase (MPO), and TNF-α were estimated. Treatment of GA and PreG attenuate PT induced thermal &mechanical hyperalgesia and allodynia symptoms along with the reduction of TBARS, total calcium, TNF-α, superoxide anion, and MPO activity levels; and decreased GSH level. Therefore, it has been concluded that GA has potential neuroprotective actions against PT induced neuropathic pain due to it's anti-oxidant, anti-inflammation and regulation of intracellular calcium ion concentration.

摘要

本研究探讨了没食子酸(GA)在紫杉醇诱导的神经性疼痛中的作用。通过给小鼠注射紫杉醇(PT:2mg/kg)来诱发神经性疼痛。连续10天静脉注射GA(20和40mg/kg)和普瑞巴林(PreG:5mg/kg)。通过评估各种疼痛测试,如丙酮滴注、针刺、足底、甩尾和夹尾试验来研究神经痛觉。在第0、4、8、12和16天评估小鼠的疼痛行为。测定坐骨神经硫代巴比妥酸反应物质(TBARS)、还原型谷胱甘肽(GSH)、超氧阴离子、钙、髓过氧化物酶(MPO)和TNF-α的水平。GA和PreG治疗可减轻PT诱导的热痛觉过敏和机械性痛觉过敏以及异常性疼痛症状,同时降低TBARS、总钙、TNF-α、超氧阴离子和MPO活性水平;并降低GSH水平。因此,得出结论:GA由于其抗氧化、抗炎和调节细胞内钙离子浓度的作用,对PT诱导的神经性疼痛具有潜在的神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b68/6562321/90e01559b940/ga1.jpg

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