Medical College, China Three Gorges University, Yichang, Hubei, People's Republic of China.
Institute of Neuroscience, Chongqing Medical University, Chongqing, People's Republic of China.
J Spinal Cord Med. 2022 Jul;45(4):595-604. doi: 10.1080/10790268.2021.1890878. Epub 2021 Apr 8.
To investigate the effect of honokiol on demyelination after compressed spinal cord injury (CSCI) and it's possible mechanism.
Animal experiment study.
Institute of Neuroscience of Chongqing Medical University.
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. 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.
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.
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.
研究和厚朴酚对压迫性脊髓损伤后脱髓鞘的影响及其可能的机制。
动物实验研究。
重庆医科大学神经科学研究所。
共 69 只 SD 大鼠随机分为 3 组:假手术组(n=15)、和厚朴酚组(n=27)和载体组(n=27)。成功建立定制压缩机致 CSCI 模型后,假手术组仅行有限椎板切除术而不压迫;和厚朴酚组行 CSCI 手术并腹腔内注射 20mg/kg 和厚朴酚;载体组行 CSCI 手术并腹腔内注射等容量生理盐水。采用 Basso、Beattie 和 Bresnahan(BBB)评分量表评估各组大鼠的运动功能。采用锇酸染色和透射电镜(TEM)检测 3 组脊髓有髓神经纤维的病理变化。免疫荧光和 Western blot 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。
载体组大鼠损伤后瘫痪痉挛,髓鞘肿胀断裂,有髓神经纤维数量减少。Western blot 分析表明,损伤后 1d 活性 caspase-3、caspase-12 和细胞色素 C 开始增加,MBP 表达逐渐减少。用和厚朴酚干预 6 天后,与载体组相比,CSCD 大鼠的运动功能和髓鞘病理变化得到改善,活性 caspase-3、caspase-12 和细胞色素 C 的表达明显降低。
和厚朴酚可能通过介导内质网-线粒体途径抑制少突胶质细胞(OLs)凋亡,改善压迫性脊髓损伤后运动功能,保护神经髓鞘脱髓鞘。