黄芩茎叶黄酮对大鼠急性脊髓损伤后的神经保护作用及对HMGB1/TLR4/NF-κB信号通路的影响

摘要

Objective:To explore the protective effect of flavonoids from stem leaf of scutellaria baicalensis georgi (SSF) on the nerve of rats with acute spinal cord injury (ASCI) and its potential molecular mechanism.Methods:Rats were divided into the sham operation group,the model group,Methylprednisolone group,SSF low dose group,SSF medium dose group and SSF high dose group,with 12 rats in each group.The spinal cord motor function (BBB) score was used to evaluate the spinal cord injury in rats;the pathological changes of spinal cord tissue were detected bv HE staining;TUNEL was used to detect the apoptosis rate of tissue cells in spinal cord injury;the expression levels of HMGB1,TLR4 and NF-κB were detected by Western blotting (WB).Results:In the model group,the spinal cord necrosis was severe;there were many cavities,and the neuron structure in gray matter was destroyed,with nuclear pyknosis.Compared with the model group,the cavity caused by necrosis was reduced in methylprednisolone group and SSF group.The BBB scores in methylprednisolone group and SSF group were significantly higher than those in the model group (P＜0.05).The apoptosis rate of spinal cord and the expression level of HMGB1,TLR4 and NF-κB in spinal cord tissue in methylprednisolone group and SSF group were significantly lower than those in model group (P＜ 0.05).The BBB score,the apoptosis rate of spinal cord cells and the expression level of HMGB1,TLR4 and NF-κB in the spinal cord of high dose group of SSF were not statistically significant,compared with those in methylprednisolone group (P＞0.05).Conclusion:SSF has a protective effect on the nerve of ASCI rats,which may be achieved by regulating the HMGB1/TLR4/NF-κB signaling pathway,and it provides a theoretical basis for the clinical treatment of ASCI.%目的 探究黄芩茎叶黄酮(SSF)对急性脊髓损伤(ASCI)大鼠神经的保护作用,及其潜在的分子作用机制.方法 将大鼠分为假手术组、模型组、甲强龙组、SSF低剂量组、SSF中剂量组、SSF高剂量组,每组12只.采用脊髓运动功能(BBB)评分法评定大鼠脊髓损伤情况,HE染色检测脊髓组织病理学变化,TUNEL检测脊髓损伤组织细胞凋亡率,蛋白质印迹法(Western blotting)检测HMGB1、Toll样受体4(TLR4)、核因子κB(NF-κB)的表达水平.结果 模型组脊髓坏死严重,出现很多空腔,灰质中神经元结构破坏,细胞核固缩;与模型组相比,甲强龙组和SSF组因坏死形成的空腔减少.甲强龙组和SSF组BBB评分显著高于模型组(P＜0.05);甲强龙组和SSF组脊髓细胞凋亡率以及脊髓组织中HMGB1、TLR4、NF-κB表达水平显著低于模型组(P＜ 0.05);SSF高剂量组BBB评分、脊髓细胞凋亡率以及脊髓组织中HMGB1、TLR4、NF-κB表达水平与甲强龙组相比,差异无统计学意义(P＞0.05).结论 SSF对ASCI大鼠神经具有保护作用,这一作用可能是通过调控HMGB1/TLR4/N F-κB信号通路实现的,为ASCI的临床治疗提供一定的理论基础.