作者: Chao Wang , Peng Wang , Wen Zeng , Weixin Li , None
DOI: 10.1016/J.BMCL.2016.01.015
关键词: Evans Blue 、 Pharmacology 、 Apoptosis 、 Oxidative stress 、 Caspase 3 、 Chemistry 、 Tetramethylpyrazine 、 LY294002 、 Proinflammatory cytokine 、 Protein kinase B
摘要: Spinal cord injury (SCI) is one of the most severe traumatic conditions, resulting in postoperative complications. Our results and other reports have shown that tetramethylpyrazine (TMP) able to exhibit neuro-protective effects after SCI. In current study, we aimed examine possible mechanism underlying effect TMP rat model improved locomotor functions decreased permeability blood-spinal barrier rats with SCI, as evidenced by increase Basso-Beattie-Bresnahan scores decrease Evans blue leakage. addition, expression several proinflammatory cytokines, including IL-1β, TNFα IL-18, reduced TUNEL-positive cells caspase 3 9 activities, thiobarbituric acid reactive substances content increased glutathione level superoxide dismutase activity rats. All these were inhibited zinc protoporphyrin IX (ZnPP), an inhibitor HO-1, LY294002, Akt. Moreover, mRNA HO-1 which was suppressed ZnPP LY294002. Akt phosphorylation but not ZnPP. Furthermore, ZnPP, significantly TMP-induced Nrf2 DNA binding promoters The data suggested induced against spinal through activation Akt/Nrf2/HO-1 signaling pathway. These appointed a new path toward understanding pathogenesis TMP-related therapy SCI associated neurodegenerative diseases.