Effect of EA on Inflammatory Response in Rat Model of LDH Based on NF-κB Signaling Pathway
Objective:To investigate effect and mechanism of electro-acupuncture(EA)on inflammatory response in rat model of lumbar disc herniation(LDH).Methods:40 SD rats were randomly divided into the control group,the model group,the sham operation group and the EA group,with 10 rats in each group.The threshold of thermal pain stimulation claw withdraw was recorded at 1 d before modeling,3 d and 7 d after modeling.The morphological changes of the lumbar spinal nerve roots were observed by HE staining;the serum levels of TNF-α,IL-1β and IL-6 were measured by ELISA;the protein and mRNA expressions of IKK-β,NF-κB p65 and IkBa in the spinal cord were detected by WB and PCR,respectively.Results:Compared with that in the pre-modeling period,the threshold of thermal pain stimulation claw withdraw was lower in the model group and the EA group 3 days after modeling,which was consistent with the characteristics of pain sensitivity in LDH,showing successful modeling;the threshold was increased in the EA group 7 days after modeling(P<0.05).EA could improve the morphological changes of lumbar spinal nerve root.Compared with those in the control group,the expressions of TNF-α,IL-1 β and IL-6 were higher in the model group and the EA group;compared with those in the model group,the expressions of TNF-α,IL-1 β and IL-6 were lower in the EA group(P<0.05).Compared with those in the control group,the protein expressions of IKK-β,NF-κB p65 and IkBa were higher in the model group and the EA group;compared with those in the model group,the protein expressions of IKK-β,NF-κB p65 and IkBa were lower in the EA group(P<0.05).Compared with those in the control group,the mRNA expressions of IKK-β,NF-κB p65 and IkBa were higher in the model group and the EA group(P<0.05);compared with those in the model group,the mRNA expressions of IKK-β,NF-κB p65 and IkBa were lower in the EA group(P<0.05).Conclusion:EA can improve inflammatory response in rats with LDH,which is possibly achieved by modulating NF-κB.