Salvianolic acid B activates Wnt/β‑catenin signaling following spinal cord injury
- Hongming Zhou
- Yi Liu
- Lei Sun
- Ming Fu
- Yao Zhao
Affiliations: 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, Department of Orthopedics, Taian City Central Hospital, Taian, Shandong 271000, P.R. China, Department of Bone Surgery, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150000, P.R. China, Department of Spine Surgery, Provincial Ear, Nose and Throat Hospital, Shandong Provincial Ear, Nose and Throat Hospital Affiliated to Shandong University, Jinan, Shandong 250012, P.R. China
- Published online on: December 5, 2019 https://doi.org/10.3892/etm.2019.8292
Copyright: © Zhou
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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.