Department of Neurosurgery, Neon Hospital, Erzincan, Turkey.
Department of Pharmacology, Erzincan Binali Yildirim University School of Medicine, Erzincan, Turkey.
Transplant Proc. 2021 Dec;53(10):3087-3092. doi: 10.1016/j.transproceed.2021.09.041. Epub 2021 Nov 10.
Ischemia is a condition in which blood flow to tissues is decreased or entirely stopped for various reasons. The reperfusion process exacerbates damage caused by ischemia in the organs and tissues. Reactive oxygen species (ROS) are mainly responsible for ischemia-reperfusion (IR) damage. ROS increase results in lipid peroxidation (LPO) and oxidative stress. In the literature, taxifolin reportedly suppresses ROS production. This study aimed to determine the effect of taxifolin, which is a flavonoid, on IR injury of the sciatic nerve in rats.
This study divided 30 albino Wistar rats into 3 groups: IR without medication (IR) group, taxifolin applied IR (TAX+IR) group, and only dissection made to the sciatic nerve sham group (SHAM). Sciatic nerve injury was induced by applying 2 hours of ischemia and 3 hours of reperfusion to the abdominal aorta and iliolumbar arteries. Biochemical and histopathologic investigations then were performed on sciatic nerve tissues. Malondialdehyde, total glutathione, glutathione reductase, and glutathione peroxidase were analyzed as oxidative stress markers, and tumor necrosis factor-α and interleukin-1β levels were evaluated as inflammatory stress markers in biochemical tests.
The IR group has statistically significantly high oxidant and cytokine levels and low antioxidant levels compared with the TAX+IR group. Taxifolin treatment was also shown to cause significant histopathologic improvement.
We suggest that taxifolin may be effective in preventing IR injury of the sciatic nerve.
缺血是由于各种原因导致组织血流减少或完全停止的一种情况。再灌注过程会加剧器官和组织中由缺血引起的损伤。活性氧（ROS）主要负责缺血再灌注（IR）损伤。ROS 增加导致脂质过氧化（LPO）和氧化应激。在文献中，报道称松属素可抑制 ROS 的产生。本研究旨在确定作为黄酮类化合物的松属素对大鼠坐骨神经 IR 损伤的影响。
本研究将 30 只白化 Wistar 大鼠分为 3 组：无药物 IR 组（IR）、应用松属素的 IR 组（TAX+IR）和仅解剖坐骨神经的假手术组（SHAM）。通过对腹主动脉和髂腰动脉施加 2 小时缺血和 3 小时再灌注来诱导坐骨神经损伤。然后对坐骨神经组织进行生化和组织病理学研究。在生化测试中，分析丙二醛、总谷胱甘肽、谷胱甘肽还原酶和谷胱甘肽过氧化物酶作为氧化应激标志物，评估肿瘤坏死因子-α和白细胞介素-1β水平作为炎症应激标志物。
与 TAX+IR 组相比，IR 组的氧化剂和细胞因子水平显著升高，抗氧化剂水平显著降低。松属素治疗还显示出显著的组织病理学改善。
我们认为松属素可能有效预防坐骨神经 IR 损伤。
