中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
42期
6813-6818
,共6页
组织构建%骨组织工程%脊髓损伤%许旺细胞%丹参%丹酚酸B%神经修复%脂多糖%核因子κB%Wnt/β-catenin%β-catenin%中药单体
組織構建%骨組織工程%脊髓損傷%許旺細胞%丹參%丹酚痠B%神經脩複%脂多糖%覈因子κB%Wnt/β-catenin%β-catenin%中藥單體
조직구건%골조직공정%척수손상%허왕세포%단삼%단분산B%신경수복%지다당%핵인자κB%Wnt/β-catenin%β-catenin%중약단체
背景：丹酚酸B是中药丹参的有效单体成分，近年已被证实有保护神经、促进神经损伤恢复的作用，但其机制尚未清楚。目的：探讨丹酚酸B对脊髓损伤大鼠许旺细胞的保护机制。方法：实验分为正常组、模型组、10μmol/L甲强龙组、丹酚酸B组(0.1，1，10，100μmol/L)。除正常组外，其他3组建立脂多糖诱导建立许旺细胞损伤模型，后2组进行对应的药物干预。以此观察丹酚酸B对脊髓损伤大鼠许旺细胞生长曲线、增殖活性、β-catenin和核因子κB蛋白与基因的表达情况。结果与结论：干预48，72，96 h，模型组细胞活性与正常组比较显著减低(P <0.01)，与模型组比较，干预72，96 h，丹酚酸B组(10μmol/L)细胞活性较模型组显著升高(P <0.05)。干预72 h时，与模型组比较，甲强龙组和丹酚酸B组许旺细胞核因子κB mRNA和蛋白表达显著降低(P <0.01)，丹酚酸B组β-catenin mRNA和蛋白表达显著升高(P <0.05)。说明丹酚酸B能够改善脂多糖刺激的大鼠许旺细胞活性损伤；同时抑制脂多糖诱导的大鼠许旺细胞核因子κB基因和蛋白的表达，促进β-catenin基因和蛋白的表达，这可能是其许旺细胞保护作用机制之一。
揹景：丹酚痠B是中藥丹參的有效單體成分，近年已被證實有保護神經、促進神經損傷恢複的作用，但其機製尚未清楚。目的：探討丹酚痠B對脊髓損傷大鼠許旺細胞的保護機製。方法：實驗分為正常組、模型組、10μmol/L甲彊龍組、丹酚痠B組(0.1，1，10，100μmol/L)。除正常組外，其他3組建立脂多糖誘導建立許旺細胞損傷模型，後2組進行對應的藥物榦預。以此觀察丹酚痠B對脊髓損傷大鼠許旺細胞生長麯線、增殖活性、β-catenin和覈因子κB蛋白與基因的錶達情況。結果與結論：榦預48，72，96 h，模型組細胞活性與正常組比較顯著減低(P <0.01)，與模型組比較，榦預72，96 h，丹酚痠B組(10μmol/L)細胞活性較模型組顯著升高(P <0.05)。榦預72 h時，與模型組比較，甲彊龍組和丹酚痠B組許旺細胞覈因子κB mRNA和蛋白錶達顯著降低(P <0.01)，丹酚痠B組β-catenin mRNA和蛋白錶達顯著升高(P <0.05)。說明丹酚痠B能夠改善脂多糖刺激的大鼠許旺細胞活性損傷；同時抑製脂多糖誘導的大鼠許旺細胞覈因子κB基因和蛋白的錶達，促進β-catenin基因和蛋白的錶達，這可能是其許旺細胞保護作用機製之一。
배경：단분산B시중약단삼적유효단체성분，근년이피증실유보호신경、촉진신경손상회복적작용，단기궤제상미청초。목적：탐토단분산B대척수손상대서허왕세포적보호궤제。방법：실험분위정상조、모형조、10μmol/L갑강룡조、단분산B조(0.1，1，10，100μmol/L)。제정상조외，기타3조건립지다당유도건립허왕세포손상모형，후2조진행대응적약물간예。이차관찰단분산B대척수손상대서허왕세포생장곡선、증식활성、β-catenin화핵인자κB단백여기인적표체정황。결과여결론：간예48，72，96 h，모형조세포활성여정상조비교현저감저(P <0.01)，여모형조비교，간예72，96 h，단분산B조(10μmol/L)세포활성교모형조현저승고(P <0.05)。간예72 h시，여모형조비교，갑강룡조화단분산B조허왕세포핵인자κB mRNA화단백표체현저강저(P <0.01)，단분산B조β-catenin mRNA화단백표체현저승고(P <0.05)。설명단분산B능구개선지다당자격적대서허왕세포활성손상；동시억제지다당유도적대서허왕세포핵인자κB기인화단백적표체，촉진β-catenin기인화단백적표체，저가능시기허왕세포보호작용궤제지일。
BACKGROUND:Salvianolic acid B is an effective monomer component of Salvia miltiorrhiza, which has been shown in recent years to have neuroprotective role and to promote nerve recovery, but its mechanism is not clear. OBJECTIVE: To explore the protective mechanism of salvianolic acid B on Schwann cels in rats with spinal cord injury. METHODS: Schwann cels of Sprague-Dawley rats were cultured and divided into normal control group, model group, 10 μmol/L methylprednisolone group and salvianolic acid B group (0.1, 1, 10, 100 μmol/L). Models of Schwann cel injury induced by lipopolysaccharide were established in al the groups except the normal control group. After intervention, growth curve and proliferative activity of Schwann cels were detected, and protein and gene expressions of β-catenin and nuclear factor-κB were observed. RESULTS AND CONCLUSION: At 48, 72, 96 hours after intervention, the cel viability of the model group was significantly lower than that of the normal control group (P < 0.01). Compared with the model group, the cel viability of salvianolic acid B group (10 μmol/L) was significantly increased at 72 and 96 hours (P < 0.05); the expressions of nuclear factor-κB protein and mRNA in the methylprednisolone group and salvianolic acid B group were declined significantly (P < 0.01), but the expressions of β-catenin mRNA and protein in the salvianolic acid B group significantly increased (P < 0.05). These results suggest that salvianolic acid B improves the viability of Schwann cels which are stimulated with lipopolysaccharide, suppresses expression of nuclear factor-κB mRNA and protein, and promotes the expression of β-catenin mRNA and protein. Above may be one of the mechanisms which salvianolic acid B protects Schwann cels.
