Spinal cord injury (SCI) is a deliberating disorder with impairments in locomotor deficits and incapacitating sensory abnormalities. Harpagophytum procumbens (Hp) is a botanical widely used for treating inflammation and pain related to various inflammatory and musculoskeletal conditions. Using a modified rodent contusion model of SCI, we explored the effects of this botanical on locomotor function and responses to mechanical stimuli, and examined possible neurochemical changes associated with SCI-induced allodynia. Following spinal cord contusion at T10 level, Hp (300 mg/kg, p.o.) or vehicle (water) was administered daily starting 24 h post-surgery, and behavioral measurements made every-other day until sacrifice (Day 21). Hp treatment markedly ameliorated the contusion-induced decrease in locomotor function and increased sensitivity to mechanical stimuli. Determination of Iba1 expression in spinal cord tissues indicated microglial infiltration starting 3 days post-injury. SCI results in increased levels of 4-hydroxynonenal, an oxidative stress product and proalgesic, which was diminished at 7 days by treatment with Hp. SCI also enhanced antioxidant heme oxygenase-1 (HO-1) expression. Concurrent studies of cultured murine BV-2 microglial cells revealed that Hp suppressed oxidative/nitrosative stress and inflammatory responses, including production of nitric oxide and reactive oxygen species, phosphorylation of cytosolic phospholipases A₂, and upregulation of the antioxidative stress pathway involving the nuclear factor erythroid 2-related factor 2 and HO-1. These results support the use of Hp for management of allodynia by providing resilience against the neuroinflammation and pain associated with SCI and other neuropathological conditions.

中文翻译：

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Harpagophytum procumbens提取物改善了大鼠脊髓损伤模型中的异常性疼痛并调节氧化和抗氧化应激途径。

脊髓损伤（SCI）是一种自发性疾病，运动​​功能障碍和感觉异常异常。夏枯草（Hp）是一种植物药，广泛用于治疗与各种炎症和肌肉骨骼疾病相关的炎症和疼痛。使用改良的SCI啮齿动物挫伤模型，我们探讨了该植物药对运动功能和对机械刺激的反应的作用，并研究了与SCI诱发的异常性疼痛相关的可能的神经化学变化。脊髓挫伤在T10水平后，在术后24小时开始每天施用Hp（300 mg / kg，口服）或溶媒（水），每隔一天进行一次行为测量，直至处死（第21天）。高压治疗显着改善了挫伤引起的运动功能下降和对机械刺激的敏感性增加。脊髓组织中Iba1表达的测定表明损伤后3天开始有小胶质细胞浸润。SCI导致4-羟基壬烯醛（一种氧化应激产物和镇痛药）水平升高，通过Hp治疗在7天时减弱。SCI还增强了抗氧化剂血红素加氧酶-1（HO-1）的表达。对培养的鼠BV-2小胶质细胞的同时研究显示，Hp抑制氧化/亚硝化应激和炎症反应，包括一氧化氮和活性氧的产生，胞质磷脂酶A的磷酸化₂，并涉及核因子类红细胞2相关因子2和HO-1的抗氧化应激途径的上调。这些结果通过提供抗SCI和其他神经病理学状况相关的神经炎症和疼痛的弹性，支持Hp用于异常性疼痛的管理。