Department of Neurosurgery, University of Health Sciences, Dışkapı Education and Research Hospital, Ankara, Turkey.
Department of Neurosurgery, Sivas Numune Hospital, Sivas, Turkey.
World Neurosurg. 2022 Nov;167:e172-e183. doi: 10.1016/j.wneu.2022.07.109. Epub 2022 Aug 7.
Dexpanthenol (DXP) reportedly protects tissues against oxidative damage in various inflammation models. This study aimed to evaluate its effects on oxidative stress, inflammation, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model.
Rabbits were randomized into 5 groups of 8 animals each: group 1 (control), group 2 (ischemia), group 3 (vehicle), group 4 (methylprednisolone, 30 mg/kg), and group 5 (DXP, 500 mg/kg). The control group underwent laparotomy only, whereas other groups were subjected to spinal cord ischemia by aortic occlusion (just caudal to the 2 renal arteries) for 20 min. After 24 h, a modified Tarlov scale was employed to record neurological examination results. Malondialdehyde and caspase-3 levels and catalase and myeloperoxidase activities were analyzed in tissue and serum samples. Xanthine oxidase activity was measured in the serum. Histopathological and ultrastructural evaluations were also performed in the spinal cord.
After SCIRI, serum and tissue malondialdehyde and caspase-3 levels and myeloperoxidase and serum xanthine oxidase activities were increased (P < 0.05-0.001). However, serum and tissue catalase activity decreased significantly (P < 0.001). DXP treatment was associated with lower malondialdehyde and caspase-3 levels and reduced myeloperoxidase and xanthine oxidase activities but increased catalase activity (P < 0.05-0.001). Furthermore, DXP was associated with better histopathological, ultrastructural, and neurological outcome scores.
This study was the first to evaluate antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of DXP on SCIRI. Further experimental and clinical investigations are warranted to confirm that DXP can be administered to treat SCIRI.
据报道，二羟丙茶碱（DXP）可保护组织免受各种炎症模型中的氧化损伤。本研究旨在评估其在实验性兔脊髓缺血再灌注损伤（SCIRI）模型中的氧化应激、炎症、细胞凋亡和神经恢复的作用。
将兔子随机分为 5 组，每组 8 只：第 1 组（对照组）、第 2 组（缺血组）、第 3 组（载体组）、第 4 组（甲泼尼龙，30mg/kg）和第 5 组（DXP，500mg/kg）。对照组仅行剖腹术，而其他组通过主动脉夹闭（位于 2 个肾动脉下方）使脊髓缺血 20min。24h 后，采用改良 Tarlov 量表记录神经检查结果。分析组织和血清样本中的丙二醛和半胱氨酸天冬氨酸蛋白酶-3 水平以及过氧化氢酶和髓过氧化物酶活性。测定血清黄嘌呤氧化酶活性。还对脊髓进行组织学和超微结构评估。
SCIRI 后，血清和组织中的丙二醛和半胱氨酸天冬氨酸蛋白酶-3 水平以及髓过氧化物酶和血清黄嘌呤氧化酶活性增加（P<0.05-0.001）。然而，血清和组织中的过氧化氢酶活性显著降低（P<0.001）。DXP 治疗与较低的丙二醛和半胱氨酸天冬氨酸蛋白酶-3 水平以及降低的髓过氧化物酶和黄嘌呤氧化酶活性但增加的过氧化氢酶活性相关（P<0.05-0.001）。此外，DXP 与更好的组织病理学、超微结构和神经功能评分相关。
本研究首次评估了 DXP 对 SCIRI 的抗氧化、抗炎、抗凋亡和神经保护作用。需要进一步的实验和临床研究来证实 DXP 可用于治疗 SCIRI。
