Objective

To investigate the effect of honokiol on demyelination after compressed spinal cord injury (CSCI) and it's possible mechanism.

Design

Animal experiment study.

Setting

Institute of Neuroscience of Chongqing Medical University.

Interventions

Total of 69 Sprague–Dawley (SD) rats were randomly divided into 3 groups: sham group (n=15), honokiol group (n=27) and vehicle group (n=27). After established CSCI model by a custom-made compressor successfully, the rats of sham group were subjected to the limited laminectomy without compression; the rats of honokiol group were subjected to CSCI surgery and intraperitoneal injection of 20 mg/kg honokiol; the rats of vehicle group were subjected to CSCI surgery and intraperitoneal injection of an equivalent volume of saline.

Outcome measures: The locomotor function of each group was assessed using the Basso, Beattie and Bresnahan (BBB) rating scale. The pathological changes of myelinated nerve fibers of spinal cord in 3 groups were detected by osmic acid staining and transmission electron microcopy (TME). Immunofluorescence and Western blot were used to research the experessions of active caspase-3, caspase-12, cytochrome C and myelin basic protein (MBP) respectively.

Results

In the vehicle group, the rats became paralyzed and spastic after injury, and the myelin sheath became swollen and broken down along with decreased number of myelinated nerve fibers. Western blot analysis manifested that active caspase-3, caspase-12 and cytochrome C began to increase 1 d after injury while the expression of MBP decreased gradually. After intervened with honokiol for 6 days, compared with the vehicle group, the locomotor function and the pathomorphological changes of myelin sheath of the CSCD rats were improved with obviously decreased expression of active caspase-3, caspase-12 and cytochrome C.

Conclusions

Honokiol may improve locomotor function and protect neural myelin sheat from demyelination via prevention oligodendrocytes (OLs) apoptosis through mediate endoplasmic reticulum (ER)-mitochondria pathway after CSCI.

中文翻译：

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厚朴酚通过调节 ER-线粒体相互作用抑制少突胶质细胞凋亡，对压缩脊髓损伤后的神经髓鞘发挥保护作用

客观的

探讨和厚朴酚对压缩性脊髓损伤(CSCI)后脱髓鞘的影响及其可能机制。

设计

动物实验研究。

环境

重庆医科大学神经科学研究所。

干预措施

将69只Sprague-Dawley（SD）大鼠随机分为3组：假手术组（n=15）、和厚朴组（n=27）和载体组（n=27）。假手术组采用特制压缩器成功建立CSCI模型后，进行无压缩的有限椎板切除术；厚朴酚组大鼠进行CSCI手术，腹腔注射厚朴酚20mg/kg；赋形剂组大鼠行CSCI手术，腹腔注射等体积生理盐水。

结果测量：使用 Basso、Beattie 和 Bresnahan (BBB) 评定量表评估每组的运动功能。采用锇酸染色和透射电子显微镜(TME)检测3组脊髓有髓神经纤维的病理变化。免疫荧光和Western印迹分别用于研究活性caspase-3、caspase-12、细胞色素C和髓鞘碱性蛋白(MBP)的表达。

结果

载体组大鼠受伤后出现瘫痪、痉挛，髓鞘肿胀、分解，有髓神经纤维数量减少。Western blot分析显示，活性caspase-3、caspase-12和细胞色素C在损伤后1 d开始升高，而MBP的表达逐渐下降。和厚朴酚干预6天后，与赋形剂组相比，CSCD大鼠的运动功能和髓鞘病理形态学改变均得到改善，活性caspase-3、caspase-12和细胞色素C的表达明显降低。

结论

和厚朴可通过介导 CSCI 后的内质网 (ER)-线粒体通路预防少突胶质细胞 (OLs) 凋亡来改善运动功能并保护神经髓鞘免受脱髓鞘。