Moini-Zanjani Taraneh, Ostad Seyed-Nasser, Labibi Farzaneh, Ameli Haleh, Mosaffa Nariman, Sabetkasaei Masoumeh
Shahid Beheshti University of Medical Sciences, Department of Pharmacology and Neuroscience Research Center, Tehran, Iran.
Tehran University of Medical Sciences, faculty of Pharmacy, Tehran, Iran.
Iran Biomed J. 2016 Nov;20(5):273-9. doi: 10.22045/ibj.2016.04. Epub 2016 Apr 25.
Evidence indicates that neuropathic pain pathogenesis is not confined to changes in the activity of neuronal systems but involves interactions between neurons, inflammatory immune and immune-like glial cells. Substances released from immune cells during inflammation play an important role in development and maintenance of neuropathic pain. It has been found that minocycline suppresses the development of neuropathic pain. Here, we evaluated the analgesic effect of minocycline in a chronic constriction injury (CCI) model of neuropathic pain in rat and assessed IL-6 concentration from cultured macrophage and microglia cells.
Male Wistar rat (n=6, 150-200 g) were divided into three different groups: 1) CCI+vehicle, 2) sham+vehicle, and 3) CCI+drug. Minocycline (10, 20, and 40 mg/kg) was injected one hour before surgery and continued daily to day 14 post ligation. Von Frey filaments and acetone, as pain behavioral tests, were used for mechanical allodynia and cold allodynia, respectively. Experiments were performed on day 0 (before surgery) and days 1, 3, 5, 7, 10, and 14 post -injury. At day 14, rats were killed and monocyte-derived macrophage from right ventricle and microglia from lumbar part of the spinal cord were isolated and cultured in RPMI and Leibovitz's media, respectively. IL-6 concentration was evaluated in cell culture supernatant after 24 h.
Minocycline (10, 20, and 40 mg/kg) attenuated pain behavior, and a decrease in IL-6 concentration was observed in immune cells compared to CCI vehicle-treated animals.
Minocycline reduced pain behavior and decreased IL-6 concentration in macrophage and microglial cells.
有证据表明,神经性疼痛的发病机制并不局限于神经元系统活动的变化,而是涉及神经元、炎性免疫细胞和免疫样神经胶质细胞之间的相互作用。炎症期间免疫细胞释放的物质在神经性疼痛的发生和维持中起重要作用。已发现米诺环素可抑制神经性疼痛的发展。在此,我们评估了米诺环素在大鼠神经性疼痛慢性缩窄损伤(CCI)模型中的镇痛作用,并测定了培养的巨噬细胞和小胶质细胞中的白细胞介素-6(IL-6)浓度。
雄性Wistar大鼠(n = 6,体重150 - 200 g)分为三组:1)CCI + 赋形剂组,2)假手术 + 赋形剂组,3)CCI + 药物组。在手术前1小时注射米诺环素(10、20和40 mg/kg),并持续每日注射至结扎后第14天。分别使用von Frey细丝和丙酮作为疼痛行为测试,用于检测机械性异常性疼痛和冷异常性疼痛。在第0天(手术前)以及损伤后第1、3、5、7、10和14天进行实验。在第14天,处死大鼠,分别从右心室分离单核细胞衍生的巨噬细胞,从脊髓腰段分离小胶质细胞,并分别在RPMI培养基和莱博维茨培养基中培养。24小时后评估细胞培养上清液中的IL-6浓度。
米诺环素(10、20和40 mg/kg)减轻了疼痛行为,与CCI赋形剂处理的动物相比,免疫细胞中的IL-6浓度降低。
米诺环素减轻了疼痛行为,并降低了巨噬细胞和小胶质细胞中的IL-6浓度。