丹酚酸B对脂多糖诱导许旺细胞损伤的保护作用机制

摘要

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.%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。