Dihydrotanshinone I Alleviates Spinal Cord Injury via Suppressing Inflammatory Response, Oxidative Stress and Apoptosis in Rats

Background: Spinal cord injury (SCI) is a serious nervous system injury, causing extremely low quality of life and immensurable economic losses. However, there is few therapies that can effectively cure the injury. The goal of the present study was to explore the potential therapeutic effects of dihydrotanshinone I (DI) for SCI and the involving mechanism. Material/Methods: A SCI rat model was structured to investigate the effects of DI on recovery of SCI. Tarlov's scale was employed to assess the neuronal function and histopathological examination was carried out by hematoxylin and eosin staining. In addition, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1 beta, inducible nitric oxide synthase (iNOS), total oxidant status (TOS) and total antioxidant status (TAS) levels were detected. Tunel assay and western blot analysis were performed to evaluate cell apoptosis. Furthermore, western blot assay was used to measure the protein expressions. Results: The results demonstrated that the treatment of DI alleviated the pathological damage induced by SCI and pro- moted the neuronal functional recovery. DI suppressed TNF-alpha, IL-1 beta, IL-6, iNOS, and TOS levels while improved the TAS level. Moreover, increased cell apoptosis in SCI rats was inhibited by administration of DI. Most importantly, DI reserved the soaring of TLR4, MyD88, HMGB1, and NOX4 level after induction of SCI. Thus, the observation revealed that the HMGB1/TLR4/NOX4 pathway may be involved in the protective effects of DI on SCI. Conclusions: In conclusion, the findings suggest that DI alleviates SCI by restraining secretion of inflammatory factors, and occurrence of oxidative stress and apoptosis in vivo. DI may be developed into an effective alternative therapy for SCI in clinic.