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首页> 外文期刊>Molecular pain >Go-sha-jinki-Gan (GJG) ameliorates allodynia in chronic constriction injury model mice via suppression of TNF-α expression in the spinal cord
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Go-sha-jinki-Gan (GJG) ameliorates allodynia in chronic constriction injury model mice via suppression of TNF-α expression in the spinal cord

机译:Go-sha-jinki-Gan(GJG)通过抑制脊髓中TNF-α的表达来改善慢性收缩损伤模型小鼠的异常性疼痛

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摘要

Alternative medicine is noted for its clinical effect and minimal invasiveness in the treatment of neuropathic pain. Go-sha-jinki-Gan, a traditional Japanese herbal medicine, has been used for meralgia and numbness in elderly patients. However, the exact mechanism of GJG is unclear. This study aimed to investigate the molecular mechanism of the analgesic effect of GJG in a chronic constriction injury model. GJG significantly reduced allodynia and hyperalgesia from the early phase (von Frey test, p?p?p?=?0.011; two-way repeated measures ANOVA). Immunohistochemistry and Western blot analysis revealed that GJG decreased the expression of Iba1 and tumor necrosis factor-α in the spinal cord. Double staining immunohistochemistry showed that most of the tumor necrosis factor-α was co-expressed in Iba1-positive cells at day 3 post-operation. GJG decreased the phosphorylation of p38 in the ipsilateral dorsal horn. Moreover, intrathecal injection of tumor necrosis factor-α opposed the anti-allodynic effect of GJG in the cold-plate test. Our data suggest that GJG ameliorates allodynia in chronic constriction injury model mice via suppression of tumor necrosis factor-α expression derived from activated microglia. GJG is a promising drug for the treatment of neuropathic pain induced by neuro-inflammation.
机译:替代药物因其在神经性疼痛治疗中的临床效果和微创性而著称。传统的日本草药Go-sha-jinki-Gan已用于治疗老年患者的疼痛和麻木。但是,GJG的确切机制尚不清楚。本研究旨在探讨GJG在慢性收缩性损伤模型中镇痛作用的分子机理。 GJG从早期就显着减少了异常性疼痛和痛觉过敏(von Frey检验,p?p?p?=?0.011;双向重复测量ANOVA)。免疫组织化学和Western blot分析显示,GJG降低了脊髓中Iba1和肿瘤坏死因子-α的表达。免疫组织化学双染色显示,术后第3天,大多数肿瘤坏死因子-α在Iba1阳性细胞中共表达。 GJG降低了同侧背角中p38的磷酸化。此外,在冷板试验中鞘内注射肿瘤坏死因子-α与GJG的抗痛觉异常作用相反。我们的数据表明,GJG可通过抑制源自活化小胶质细胞的肿瘤坏死因子-α表达来改善慢性收缩损伤模型小鼠的异常性疼痛。 GJG是一种有前途的药物,可用于治疗由神经炎症引起的神经性疼痛。

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