Department of Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250014, Shandong, China.
Comput Intell Neurosci. 2022 May 11;2022:7619797. doi: 10.1155/2022/7619797. eCollection 2022.
Spinal cord reperfusion injury as a secondary damage after primary spinal cord injury is an important factor causing nerve cell damage. In this study, we aim to investigate the effects and mechanisms of tanshinone (TAE) in the rabbit spinal cord during ischemia-reperfusion. New Zealand white rabbits were randomly divided into 3 groups: sham-operated group (5 rabbits), ischemia-reperfusion group (0.9% TAE was administered intraperitoneally 30 min before ischemia, and 4 groups of 5 rabbits each according to different time periods of reperfusion: group A reperfused for 0.5 h, group B reperfused for 2 h, group C reperfused for 8 h, and group reperfused for 24 h), and TAE group (an ischemia-reperfused for 24 h). Group A was reperfused for 0.5 h, group B for 2 h, group C for 8 h, group for 24 h, and group TAE (TAE was applied 30 min before ischemia reperfusion, grouped as ischemia-reperfusion group). The expression of JNK (c-Jun NH2-terminal Kinase) and phosphorylation-JNK (p-JNK) in spinal cord tissues of each group were detected by Western blot. Light and electron microscopy showed that early apoptosis started in group B in the ischemia-reperfusion group, while early apoptosis appeared only in group in the tanshinone intervention group. Western blot showed that p-JNK expression started in group B in the ischemia-reperfusion group and gradually increased with the prolongation of ischemia time, while p-JNK expression only increased in group in the tanshinone intervention group. In the tanshinone intervention group, p-JNK was activated only in group and its activity was less than that in the ischemia-reperfusion group; the protein expression of JNK did not change significantly in both groups. Spinal cord ischemia-reperfusion can cause spinal cord injury by activating the signaling molecule JNK (MRPKs family), and early tanshinone intervention can partially inhibit this injury. Our finding provides a new idea and theoretical basis for clinical treatment of spinal cord ischemia-reperfusion injury.
脊髓再灌注损伤是原发性脊髓损伤后的继发性损伤，是导致神经细胞损伤的重要因素。本研究旨在探讨丹参酮（TAE）在兔脊髓缺血再灌注中的作用及机制。新西兰白兔随机分为 3 组：假手术组（5 只）、缺血再灌注组（缺血前 30min 腹腔注射 0.9%TAE，每组 5 只，根据再灌注时间不同分为 4 组：A 组再灌注 0.5h、B 组再灌注 2h、C 组再灌注 8h、D 组再灌注 24h）和 TAE 组（再灌注 24h）。A 组再灌注 0.5h，B 组再灌注 2h，C 组再灌注 8h，D 组再灌注 24h，TAE 组（缺血前 30min 给予 TAE，分组为缺血再灌注组）。Western blot 检测各组脊髓组织 JNK（c-Jun NH2-terminal Kinase）和磷酸化-JNK（p-JNK）的表达。光镜和电镜显示，缺血再灌注组 B 组出现早期凋亡，丹参酮干预组仅 D 组出现早期凋亡。Western blot 显示，缺血再灌注组 B 组 p-JNK 表达开始，并随缺血时间延长逐渐升高，而丹参酮干预组仅 D 组 p-JNK 表达升高。在丹参酮干预组中，p-JNK 仅在 D 组激活，其活性低于缺血再灌注组；两组 JNK 蛋白表达均无明显变化。脊髓缺血再灌注可通过激活信号分子 JNK（MRPKs 家族）引起脊髓损伤，早期丹参酮干预可部分抑制这种损伤。本研究为临床治疗脊髓缺血再灌注损伤提供了新的思路和理论依据。
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