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硫酸软骨素通过增加抗炎分子和减少氧化应激,对大鼠慢性压迫性损伤诱导的神经性疼痛产生抗伤害感受和神经保护作用。

Chondroitin sulfate produces antinociception and neuroprotection in chronic constriction injury-induced neuropathic pain in rats by increasing anti-inflammatory molecules and reducing oxidative stress.

作者信息

Olaseinde Olutayo Folajimi, Owoyele Bamidele Victor

机构信息

Department of Physiology, Neuroscience and Inflammation Unit, College of Health Sciences, University of Ilorin, Ilorin, Kwara State, Nigeria.

出版信息

Int J Health Sci (Qassim). 2021 Sep-Oct;15(5):3-17.

Abstract

OBJECTIVES

Damage to the peripheral and central nervous system lead to Neuropathic pain (NP) which is a widespread and devitalizing condition. chondroitin sulfate (CS), has been used in managing joint pain and osteoarthritis. In this study, the effectiveness of CS on NP induced by chronic constriction injury (CCI) is examined.

METHODS

Thirty Wistar rats were distributed at random into six groups ( = 5). Sciatic nerve ligation was carried out by encircling the nerve with four loose ligatures to induce NP. Allodynia (cold and mechanical) and heat hyperalgesia were assessed using Acetone, von Frey filament and Hot plate tests. CCI induction resulted to NP, prominent from the 3 day after surgery. tructural architecture of sciatic nerves was evaluated via histological examination of the transverse section of the nerves.

RESULTS

Oral administration of CS (600 mg/kg and 900 mg/kg for 21 days) resulted in significant ( < 0.05) inhibition of allodynia (cold and mechanical) and thermal hyperalgesia. Lipid peroxidation, tumor necrosis factor-α (TNF-α), calcitonin gene related peptide (CGRP), C reactive protein (CRP), and oxidative stress were attenuated by CS. CS also improved interleukin (IL)-6, nitric oxide (NO), total antioxidant capacity (TAC).

CONCLUSION

These findings suggest that CS attenuates allodynia, and thermal hyperalgesia induced by CCI by downregulating TNF-α, CRP, CGRP, oxidative enzymes, and upregulating IL-6, NO, and TAC. Nociceptive behavioral studies and histological findings showed significant improvement in the CS treated groups compared to CCI rats. These findings are responsible for the beneficial effect of CS in NP.

摘要

目的

外周和中枢神经系统损伤会导致神经性疼痛(NP),这是一种普遍且使人衰弱的病症。硫酸软骨素(CS)已被用于治疗关节疼痛和骨关节炎。在本研究中,考察了CS对慢性压迫性损伤(CCI)诱导的NP的疗效。

方法

将30只Wistar大鼠随机分为6组(每组n = 5)。通过用四根松结扎环绕坐骨神经来诱导NP。使用丙酮、von Frey细丝和热板试验评估痛觉过敏(冷觉和机械觉)和热痛觉过敏。CCI诱导导致NP,从手术后第3天开始明显。通过对神经横切面进行组织学检查来评估坐骨神经的结构。

结果

口服CS(600mg/kg和900mg/kg,持续21天)可显著(P < 0.05)抑制痛觉过敏(冷觉和机械觉)和热痛觉过敏。CS可减轻脂质过氧化、肿瘤坏死因子-α(TNF-α)、降钙素基因相关肽(CGRP)、C反应蛋白(CRP)和氧化应激。CS还可改善白细胞介素(IL)-6、一氧化氮(NO)、总抗氧化能力(TAC)。

结论

这些发现表明,CS通过下调TNF-α、CRP、CGRP和氧化酶,并上调IL-6、NO和TAC,减轻CCI诱导的痛觉过敏和热痛觉过敏。伤害性行为学研究和组织学结果显示,与CCI大鼠相比,CS治疗组有显著改善。这些发现解释了CS在NP中的有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37b/8434845/ca2d3ccaa51b/IJHS-15-3-g001.jpg

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