补肝健腰方对腰椎间盘突出大鼠NF-κB信号通路的影响

Effect of Bugan Jianyao Decoction(补肝健腰方) on NF-κB Signal Pathway in Rats with Lumbar Disc Herniation

目的:观察补肝健腰方对腰椎间盘突出大鼠NF-κB信号通路的影响。方法:取SD大鼠100只,随机分为正常对照组、假手术组、模型对照组、补肝健腰方组、塞来昔布组各20只。补肝健腰方组、塞来昔布组制备大鼠腰椎间盘突出模型成功后分别予补肝健腰方、塞来昔布灌胃。干预前、干预后第1、2、3周,各组随机选取5只大鼠处死,检测核因子κB(NF-κB)mRNA、IκB激酶β(IKK-β)mRNA以及下游产物肿瘤坏死因子α(TNF-α)的表达。结果:在干预前,补肝健腰方组、塞来昔布组大鼠腰椎间盘突出局部组织NF-κBmRNA、IKK-βmRNA及TNF-α表达与模型对照组比较,差异无统计学意义(P>0.05);干预第1、2、3周,补肝健腰方组大鼠NF-κBmRNA、IKK-βmRNA及TNF-α表达均低于模型对照组(P<0.05)。补肝健腰方组大鼠干预第1、2、3周的NF-κBmRNA、IKK-βmRNA及TNF-α表达均低于干预前(P<0.05)。结论:补肝健腰方具有调控腰椎间盘突出大鼠NF-κB信号通路的作用,可减少NF-κBmRNA、IKK-βmRNA及TNF-α表达,这可能为其治疗腰椎间盘突出症的作用机制。

Objective:To observe the effect of Bugan Jianyao decoction on NF-κB signal pathway in rats with lumbar disc herniation.Method:The 100 SD rats were randomly divided into normal control group,shamoperated group,model control group,Bugan Jianyao decoction rgoup and celecoxib group,each group with 20 rats.After lumbar disc herniation model was prepared successfully,Bugan Jianyao decoction group were gived the Bugan Jianyao decoction intragastric administration,while celecoxib group was given celecoxib,normal control group,sham-operated group,model control group were intragastrically administrated with the same dose of saline.NF-κB,IKK-βmRNA and TNF-αexpression were detected at 1st,2nd,3rd week.Results:Before intervention,the expressions of NF-κB,IKK-βand TNF-αin the local tissues of lumbar disc herniation in Bugan Jianyao decoction group and celecoxib group were not significantly different from those in model control group(P>0.05).The expression of NF-κB,IKK-βand TNF-αin Bugan Jianyao decoction group was lower than that in model control group at the 1st,2nd and 3rd week after intervention(P<0.05).The expression of NF-κB,IKK-βand TNF-αin Bugan Jianyao decoction group was lower than that before intervention at the 1st,2nd and 3rd week(P<0.05).Conclusions:Bugan Jianyao decoction has the effect of regulating the NF-κB signaling pathway,and reducing NF-κB,IKK-βmRNA and TNF-αexpression,it may be a mechanism for the treatment of lumbar disc herniation.