King's Lab, School of Pharmacy, Shanghai Jiao Tong University, Shanghai, 200240, China.
School of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China; King's Lab, School of Pharmacy, Shanghai Jiao Tong University, Shanghai, 200240, China.
Biochem Biophys Res Commun. 2020 May 14;525(4):1087-1094. doi: 10.1016/j.bbrc.2020.03.023. Epub 2020 Mar 14.
Lemairamin (also known as wgx-50), is isolated from the pericarps of the Zanthoxylum plants. As an agonist of α7 nicotinic acetylcholine receptors (α7nAChRs), it can reduce neuroinflammation in Alzheimer's disease. This study evaluated its antinociceptive effects in pain hypersensitivity and explored the underlying mechanisms. The data showed that subcutaneous lemairamin injection dose-dependently inhibited formalin-induced tonic pain but not acute nociception in mice and rats, while intrathecal lemairamin injection also dose-dependently produced mechanical antiallodynia in the ipsilateral hindpaws of neuropathic and bone cancer pain rats without affecting mechanical thresholds in the contralateral hindpaws. Multiple bi-daily lemairamin injections for 7 days did not induce mechanical antiallodynic tolerance in neuropathic rats. Moreover, the antinociceptive effects of lemairamin in formalin-induced tonic pain and mechanical antiallodynia in neuropathic pain were suppressed by the α7nAChR antagonist methyllycaconitine. In an α7nAChR antagonist-reversible manner, intrathecal lemairamin also stimulated spinal expression of IL-10 and β-endorphin, while lemairamin treatment induced IL-10 and β-endorphin expression in primary spinal microglial cells. In addition, intrathecal injection of a microglial activation inhibitor minocycline, anti-IL-10 antibody, anti-β-endorphin antiserum or μ-opioid receptor-preferred antagonist naloxone was all able to block lemairamin-induced mechanical antiallodynia in neuropathic pain. These data demonstrated that lemairamin could produce antinociception in pain hypersensitivity through the spinal IL-10/β-endorphin pathway following α7nAChR activation.
柠檬酰胺(也称为 wgx-50)是从花椒属植物的果皮中分离出来的。作为α7 烟碱型乙酰胆碱受体(α7nAChR)的激动剂,它可以减轻阿尔茨海默病中的神经炎症。本研究评估了其在疼痛过敏中的镇痛作用,并探讨了潜在的机制。研究数据显示,皮下注射柠檬酰胺可剂量依赖性地抑制福尔马林诱导的强直性疼痛,但不影响小鼠和大鼠的急性痛觉,鞘内注射柠檬酰胺也可剂量依赖性地产生神经性痛觉过敏和骨癌痛大鼠的同侧后足机械性抗痛觉过敏,而不影响对侧后足的机械阈值。多次每日两次柠檬酰胺注射 7 天不会诱导神经性痛觉过敏大鼠的机械性抗痛觉过敏耐受。此外,柠檬酰胺在福尔马林诱导的强直性疼痛和神经性疼痛的机械性抗痛觉过敏中的镇痛作用被 α7nAChR 拮抗剂甲基-六氢-罂粟碱抑制。以 α7nAChR 拮抗剂可逆的方式,鞘内注射柠檬酰胺也刺激脊髓白细胞介素-10 和β-内啡肽的表达,而柠檬酰胺处理诱导初级脊髓小胶质细胞中白细胞介素-10 和β-内啡肽的表达。此外,鞘内注射小胶质细胞激活抑制剂米诺环素、抗白细胞介素-10 抗体、抗β-内啡肽抗血清或μ-阿片受体优先拮抗剂纳洛酮均可阻断柠檬酰胺诱导的神经性疼痛的机械性抗痛觉过敏。这些数据表明,柠檬酰胺通过激活α7nAChR 后脊髓白细胞介素-10/β-内啡肽途径产生疼痛过敏中的镇痛作用。