Zhou Hongming, Liu Yi, Sun Lei, Fu Ming, Zhao Yao
Department of Emergency Trauma Surgery, Linyi City Central Hospital, Linyi, Shandong 276400, P.R. China.
Department of Bone Surgery, Linyi City Central Hospital, Linyi, Shandong 276400, P.R. China.
Exp Ther Med. 2020 Feb;19(2):825-832. doi: 10.3892/etm.2019.8292. Epub 2019 Dec 5.
Neural cell apoptosis serves a key role in spinal cord injury (SCI), which is a threat to human health. The present study aimed to evaluate the neuroprotective mechanism of salvianolic acid B (Sal B) in a spinal cord injury (SCI) rat model. Basso, Beattie, and Bresnahan scores demonstrated that Sal B treatment significantly increased locomotor functional recovery in SCI rats compared with SCI model rats between 3 and 8 weeks. Nissl staining demonstrated that Sal B enhanced motor neuron survival and decreased lesion size after SCI. Reverse transcription-quantitative PCR analysis demonstrated that Sal B treatment significantly enhanced the mRNA levels of lymphoid enhancer biding factor-1 and HNF1 homeobox A. In addition, Sal B treatment enhanced the expression of β-catenin. Western blot analysis determined that Sal B treatment significantly decreased the expression of pro-apoptosis proteins, including Bax, cleaved caspase-3 and -9, in spinal cord tissues after SCI but enhanced the expression of Bcl-2, an anti-apoptotic protein. Furthermore, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining demonstrated that, compared with the SCI group, Sal B treatment decreased the number of TUNEL-positive neurons. In summary, the present study produced novel data demonstrating the neuroprotective effect of Sal B on SCI with the mechanism likely primarily mediated via the Wnt/β-catenin signaling pathway. The present findings may be of potential therapeutic value for future SCI treatments.
神经细胞凋亡在脊髓损伤（SCI）中起关键作用，而脊髓损伤对人类健康构成威胁。本研究旨在评估丹酚酸B（Sal B）在脊髓损伤（SCI）大鼠模型中的神经保护机制。Basso、Beattie和Bresnahan评分表明，与SCI模型大鼠相比，Sal B治疗在3至8周内显著提高了SCI大鼠的运动功能恢复。尼氏染色表明，Sal B可增强运动神经元存活并减小SCI后的损伤大小。逆转录-定量PCR分析表明，Sal B治疗显著提高了淋巴增强因子结合因子-1和肝细胞核因子1同源框A的mRNA水平。此外，Sal B治疗增强了β-连环蛋白的表达。蛋白质印迹分析确定，Sal B治疗显著降低了SCI后脊髓组织中促凋亡蛋白（包括Bax、裂解的半胱天冬酶-3和-9）的表达，但增强了抗凋亡蛋白Bcl-2的表达。此外，末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色表明，与SCI组相比，Sal B治疗减少了TUNEL阳性神经元的数量。总之，本研究产生了新的数据，证明Sal B对SCI具有神经保护作用，其机制可能主要通过Wnt/β-连环蛋白信号通路介导。本研究结果可能对未来SCI治疗具有潜在的治疗价值。
