OBJECTIVE To investigate the effects and mechanism of Yiqi huoxue decoction(YQHX)on lumbar disc herniation in rats.METHODS Rats were randomly divided into sham operation group,model group,NF-κB inhibitor group(QNZ group,1 mg/kg),YQHX group(9.1 g/kg)and combination group(YQHX+QNZ group,the same dose as each single drug group),with 10 rats in each group.Except for sham operation group,lumbar disc herniation model of rats was induced in other groups;administration groups were given QNZ intraperitoneally or/and YQHX intragastrically,once a day,for 8 consecutive weeks.The severity of intervertebral disc herniation was evaluated in each group;the pathological changes of intervertebral discs and the changes of autophagy of nucleus pulposus cells were all observed;the level of tumor necrosis factor-α(TNF-α)in serum,and the ratios of Bcl-2/adenovirus E1B interacting protein 3(BNIP3)and Beclin-1 positive cells in intervertebral disc tissues were detected;the phosphorylation of nuclear factor-κB(NF-κB)p65,the expressions of tumor necrosis factor receptor-associated factor-2(TRAF-2),TRAF-3,BNIP3 and LC3B protein,and mRNA expressions of NF-κB p65,LC3B,p62,BNIP3 and Beclin-1 were determined.RESULTS Compared with model group,Pfirrmann grading score decreased significantly,the pathological injury of intervertebral disc tissue was relieved in YQHX group;the number of autophagosomes in nucleus pulposus cells increased;serum level of TNF-α and mRNA expression of p62 in intervertebral disc tissue decreased significantly;the ratios of BNIP3 and Beclin-1 positive cells,the phosphorylation of NF-κB p65,the expressions of TRAF-2,TRAF-3,BNIP3 and LC3B protein as well as the mRNA expressions of NF-κB p65,LC3B,BNIP3 and Beclin-1 decreased significantly in intervertebral disc tissues(P＜0.05).The changes of above indexes in YQHX group were reversed partly in YQHX+QNZ group.CONCLUSIONS YQHX promotes the elevation of autophagy level of intervertebral discs,slows down the inflammatory response and the progression of lumbar disc herniation by activating the NF-κB signaling pathway.
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