Research Center of Physiology, Semnan University of Medical Sciences, Semnan 3519899951, Iran.
Department of Physiology, Faculty of Medicine, Semnan University of Medical Sciences, Semnan 3519899951, Iran.
ScientificWorldJournal. 2020 Nov 25;2020:4046256. doi: 10.1155/2020/4046256. eCollection 2020.
Crocin as an important constituent of saffron has antineuropathic pain properties; however, the exact mechanism of this effect is not known. The aim of this study was whether the hypoalgesic effect of crocin can be exerted through muscarinic receptors.
In the present project, 36 male Wistar rats (200 ± 20 g) were used. Animals randomly divided into six groups (sham, neuropathy, neuropathy + crocin, neuropathy + atropine 0.5 mg/kg, neuropathy + atropine 1 mg/kg, and neuropathy + atropine 1 mg/kg + crocin). Neuropathy was induced by the chronic constriction injury (CCI) method on the sciatic nerve. Crocin and atropine was administered intraperitoneally during 14 days following the 14 day after surgery. Pain response was detected every three days, two hours after each injection and 3 days following last injection. Mechanical allodynia and thermal hyperalgesia were detected using the Von Frey filaments and plantar test device, respectively.
CCI significantly reduced the paw withdrawal response to mechanical and thermal stimulus ( < 0.01 and < 0.05, respectively). Crocin therapy significantly reduced mechanical allodynia and thermal hyperalgesia induced by CCI ( < 0.05). Atropine pretreatment significantly blocked the hypoalgesic effect of crocin ( < 0.05 in mechanical allodynia and < 0.01 in thermal hyperalgesia). Fourteen days administration of atropine alone at a dose of 0.5 mg/kg but not 1 mg/kg significantly reduced CCI-induced mechanical allodynia at day 30 after surgery.
Crocin significantly decreased CCI-induced neuropathic pain. The hypoalgesic effect of crocin was blocked by atropine pretreatment, which indicates an important role for muscarinic receptors in the effect of crocin.
西红花中的主要成分藏红花酸具有抗神经病理性疼痛的特性；然而，其确切的作用机制尚不清楚。本研究旨在探讨藏红花的镇痛作用是否可以通过毒蕈碱受体发挥作用。
本项目使用了 36 只雄性 Wistar 大鼠（200±20g）。动物随机分为六组（假手术组、神经病变组、神经病变+藏红花组、神经病变+阿托品 0.5mg/kg 组、神经病变+阿托品 1mg/kg 组和神经病变+阿托品 1mg/kg+藏红花组）。通过坐骨神经慢性缩窄性损伤（CCI）方法诱导神经病变。藏红花和阿托品在手术后第 14 天开始腹腔注射，共 14 天。在每次注射后 2 小时和最后一次注射后 3 天，每隔三天检测疼痛反应。使用 Von Frey 细丝和足底测试装置检测机械性痛觉过敏和热痛觉过敏。
CCI 显著降低了机械和热刺激引起的足底退缩反应（分别为<0.01 和<0.05）。藏红花治疗显著降低了 CCI 诱导的机械性痛觉过敏和热痛觉过敏（分别为<0.05）。阿托品预处理显著阻断了藏红花的镇痛作用（机械性痛觉过敏为<0.05，热痛觉过敏为<0.01）。单独给予 0.5mg/kg 剂量的阿托品 14 天，而不是 1mg/kg，可显著降低术后第 30 天 CCI 诱导的机械性痛觉过敏。
藏红花显著降低了 CCI 诱导的神经病理性疼痛。藏红花的镇痛作用被阿托品预处理阻断，表明毒蕈碱受体在藏红花的作用中起重要作用。
