Department of Neurosurgery, Van Education and Research Hospital, Van, Turkey.
Faculty of Medicine, Department of Neurosurgery, Kirikkale University, Kırıkkale, Turkey.
Injury. 2022 Nov;53(11):3624-3635. doi: 10.1016/j.injury.2022.08.061. Epub 2022 Aug 30.
Proinflammatory cytokines released from nerve endings and surrounding injured tissue after nerve damage can prolong the inflammation process, delay nerve healing or result in poor quality nerve healing. In this case, due to the loss of function in the muscles innervated by the damaged nerve, the patient may have neurological and functional difficulties which may reduce the patient's quality of life and create an economic burden. Although the attempts of many pharmacological agents to heal crush injury of peripheral nerves have been recorded in literature, a drug that can provide adequate recovery of the crushed nerve and can be applied in daily life has not been defined as yet. This study aimed to assess the effects of calcium dobesilate on sciatic nerve crush injury in a rat model.
A total of 26 male Wistar albino rats were separated into four groups as follows: CONTROL group (healthy subjects, n=6); SHAM group (crush injury was created, n=6); MP group (after created crush injury, methylprednisolone was administered, n=7); and CAD group (after created crush injury, calcium dobesilate was administered, n=7). A crush injury was created, then the electrophysiological findings and sciatic nerve functional index (SFI) were recorded before euthanasia. After the euthanasia of all the rats, samples of the crushed nerve and gastrocnemius muscle were evaluated histopathologically, immunohistochemically, and biochemically.
Both pharmacological agents were histopathologically effective in axon regeneration and repair. Calcium dobesilate did not preserve total muscle mass but was seen to prevent atrophy microscopically. Immunohistochemistry and biochemistry results showed that calcium dobesilate and methylprednisolone had anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-autophagic activity in the crushed sciatic nerve. Neither calcium dobesilate nor methylprednisolone improved the nerve conductance level. SFI values obtained on day 30 from the CAD group were numerically closer to the values of the healthy animals but not at a statistically significant level.
The study results demonstrated that calcium dobesilate could suppress inflammatory processes and provide histopathological and functional improvements in the injured nerve in rats. Therefore, further clinical studies are recommended to investigate in detail the therapeutic effects of calcium dobesilate on peripheral nerve crush injury.
神经损伤后，从神经末梢和周围受损组织释放的促炎细胞因子可以延长炎症过程，延迟神经愈合或导致神经愈合质量差。在这种情况下，由于受损神经支配的肌肉功能丧失，患者可能会出现神经和功能障碍，这可能会降低患者的生活质量并造成经济负担。尽管文献中有许多药理学药物试图治愈周围神经挤压伤，但尚未确定一种能够提供足够的挤压神经恢复并可在日常生活中应用的药物。本研究旨在评估钙波司他汀对大鼠坐骨神经挤压伤的影响。
将 26 只雄性 Wistar 白化大鼠分为四组：对照组（健康受试者，n=6）；SHAM 组（造成挤压伤，n=6）；MP 组（造成挤压伤后，给予甲基强的松龙，n=7）；和 CAD 组（造成挤压伤后，给予钙波司他汀，n=7）。在安乐死前，先建立挤压伤，然后记录电生理发现和坐骨神经功能指数（SFI）。所有大鼠安乐死后，评估挤压神经和腓肠肌的组织病理学、免疫组织化学和生物化学。
两种药物在轴突再生和修复方面均具有组织病理学作用。钙波司他汀不能保持总肌肉质量，但在显微镜下可以防止萎缩。免疫组织化学和生物化学结果表明，钙波司他汀和甲基强的松龙在挤压的坐骨神经中具有抗炎、抗氧化、抗细胞凋亡和抗自噬作用。钙波司他汀和甲基强的松龙均未改善神经传导水平。CAD 组第 30 天的 SFI 值在数值上更接近健康动物的值，但无统计学意义。
研究结果表明，钙波司他汀可抑制炎症过程，为大鼠受损神经提供组织病理学和功能改善。因此，建议进行进一步的临床研究，详细研究钙波司他汀对周围神经挤压伤的治疗作用。
