Student Research Committee, Sabzevar University of Medical Sciences, Sabzevar, Iran.
Department of Internal Medicine, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran.
Acta Neuropsychiatr. 2022 Oct;34(5):260-268. doi: 10.1017/neu.2022.3. Epub 2022 Feb 3.
This study was aimed at evaluating the efficacy of glucosamine and potential mechanisms of actions in a neuropathic pain model in rats.
Glucosamine (500, 1000 and 2000 mg/kg) was administered via gavage route, 1 day before the chronic constriction injury (CCI) of sciatic nerve and daily for 14 days (prophylactic regimen), or from days 5 to 14 post-injury (therapeutic regimen), as the indicators of neuropathic pain, mechanical allodynia, cold allodynia and thermal hyperalgesia were assessed on days 0, 3, 5, 7, 10 and 14 after ligation. Inducible nitric oxide synthase (iNOS) and tumour necrosis factor alpha (TNF-α) gene expressions were measured by real-time polymerase chain reaction. TNF-α protein content was measured using the enzyme-linked immunosorbent assay method.
Three days after nerve injury, the threshold of pain was declined among animals subjected to neuropathic pain. Mechanical and cold allodynia, as well as thermal hyperalgesia were attenuated by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. However, existing pain was not decreased by this drug. Increased mRNA expression of iNOS and TNF-α was significantly reduced in the spinal cord of CCI animals by glucosamine (500, 1000, 2000 mg/kg) in the prophylactic regimen. The overall expression of spinal TNF-α was increased by CCI, but this increase was reduced in animals receiving glucosamine prophylactic treatment.
Findings suggest that glucosamine as a safe supplement may be a useful candidate in preventing neuropathic pain following nerve injury. Antioxidant and anti-inflammatory effects may be at least in part responsible for the antinociceptive effects of this drug.
本研究旨在评估葡萄糖胺在大鼠神经病理性疼痛模型中的疗效及其潜在作用机制。
通过灌胃途径给予葡萄糖胺（500、1000 和 2000mg/kg），在坐骨神经慢性缩窄损伤（CCI）前 1 天开始给药，每天给药 14 天（预防方案），或在损伤后第 5 天至第 14 天给药（治疗方案），以评估神经病理性疼痛的指标，包括机械性痛觉过敏、冷感觉过敏和热痛觉过敏，在结扎后第 0、3、5、7、10 和 14 天进行评估。通过实时聚合酶链反应测量诱导型一氧化氮合酶（iNOS）和肿瘤坏死因子-α（TNF-α）基因表达。通过酶联免疫吸附测定法测量 TNF-α 蛋白含量。
神经损伤后 3 天，神经病理性疼痛动物的疼痛阈值下降。葡萄糖胺（500、1000、2000mg/kg）在预防方案中减轻了机械性和冷感觉过敏以及热痛觉过敏。然而，该药物并没有减轻现有的疼痛。葡萄糖胺（500、1000、2000mg/kg）在预防方案中显著降低了 CCI 动物脊髓中 iNOS 和 TNF-α 的 mRNA 表达。CCI 导致脊髓 TNF-α 的总体表达增加，但接受葡萄糖胺预防治疗的动物中这种增加减少了。
研究结果表明，葡萄糖胺作为一种安全的补充剂，可能是预防神经损伤后神经病理性疼痛的有用候选药物。抗氧化和抗炎作用可能至少部分解释了该药物的镇痛作用。
