CAJ | 학술논문

目的：研究雷帕霉素减弱碱性成纤维细胞生长因子（ bFGF）对急性脊髓损大鼠后肢功能恢复的作用分子机制。方法 SD大鼠随机分为假手术组、模型组、单用药组（80μg · kg－1 bFGF ）、联合用药组（80μg · kg－1 bFGF 和4 mg· kg－1雷帕霉素），连续给药7天后处死。BBB法进行后肢运动功能评分，HE染色观察脊髓损伤组织学变化， Western blot 法检测自噬系统LC3、泛素化蛋白Ub、p62的表达。结果术后3 d开始，联合用药组BBB评分明显低于单用药组；单用药组脊髓组织结构明显比联合用药组致密；与单用药组相比，联合给药组LC3、Ub表达量上升，而p62表达下降。结论雷帕霉素通过调节自噬和泛素化蛋白降解系统来减弱bFGF对脊髓损伤大鼠后肢功能恢复。
목적：연구뢰파매소감약감성성섬유세포생장인자（ bFGF）대급성척수손대서후지공능회복적작용분자궤제。방법 SD대서수궤분위가수술조、모형조、단용약조（80μg · kg－1 bFGF ）、연합용약조（80μg · kg－1 bFGF 화4 mg· kg－1뢰파매소），련속급약7천후처사。BBB법진행후지운동공능평분，HE염색관찰척수손상조직학변화， Western blot 법검측자서계통LC3、범소화단백Ub、p62적표체。결과술후3 d개시，연합용약조BBB평분명현저우단용약조；단용약조척수조직결구명현비연합용약조치밀；여단용약조상비，연합급약조LC3、Ub표체량상승，이p62표체하강。결론뢰파매소통과조절자서화범소화단백강해계통래감약bFGF대척수손상대서후지공능회복。
Objective To investigate the mechanisms of rapamycin re-ducing basic fibroblast growth factor ( bFGF) to promote hind limbs func-tional recovery in rats with spinal cord injury .Methods SD rats were randomly divided into sham group , model group , single drug group ( 80μg · kg -1 bFGF ) , combination group ( 80 μg · kg -1 bFGF and 4 mg· kg-1 rapamycin),the rats were sacrificed at 7 days after continuous injection of drug delivery .The nerve function of hind limb motor was e-valuated by Basso, Beattie, and Bresnahan(BBB) scores.Histological changes of injured spinal cords were observed by haematoxylin and eosin ( HE) staining.The expression protein of autophagy related protein mi-crotubule-associated protein 1 light chain 3 ( LC3 ) , ubiquitinated rela-ted proteins Ub and p62 were analysised by Western blot .Results Three days after postinjury , BBB scores of the combination group were lower than the single drug group .HE staining showed that spinal cord tissue structure of the single drug group were more dense than the combination group . Western blot results showed that expression of LC 3 and Ub were signifi-cantly increased in the combination group than in those in single drug group , while the expression of p 62 went down in the combination group than in those in single drug group group .Conclusion Rapamycinreduced bFGF promote functional recovery in rats with spinal cord injury by regula -ting autophagy and ubiquitinated proteins .