非压迫性椎间盘髓核突出所致神经根损伤大鼠血清白细胞介素23、白细胞介素17的表达水平及意义

Expression levels and significance of serum interleukin 23 and interleukin 17 in rats with nerve root injury caused by non-compressive herniated nucleus pulposus

目的探讨非压迫性椎间盘髓核突出所致神经根损伤大鼠血清白细胞介素(IL)-23、IL-17的表达水平及意义。方法将48只雄性SD大鼠随机分成实验组、对照组,每组24只。实验组大鼠建立非压迫性椎间盘髓核突出模型。分别于造模后1周、3周、5周时,每组随机抽取8只大鼠,测定大鼠右后肢疼痛缩爪阈值以及血清IL-17、IL-23水平,并观察腰椎神经根组织形态学变化。结果术后1周、3周时,实验组大鼠的右后肢疼痛缩爪阈值均低于对照组,血清中IL-23与IL-17水平均高于对照组(均P<0.05),而术后5周时,两组大鼠的右后肢缩爪阈值及血清IL-23、IL-17水平差异均无统计学意义(均P>0.05)。苏木精-伊红染色结果显示,对照组大鼠术后腰椎神经纤维排列规律,大小基本一致,髓鞘完整,呈红色,位于轴突周围,未发现变性改变和炎症细胞浸润;实验组大鼠术后1周时腰椎神经根纵切面可见神经纤维髓鞘部分崩解、呈空泡病变及炎症细胞浸润,术后3周时神经根损伤加重,而术后5周时神经根基本恢复正常。结论非压迫性椎间盘髓核突出导致的神经根损伤大鼠血清中IL-17、IL-23的表达水平增高,IL-23/IL-17炎症轴可能在根性神经根痛发病过程起关键作用。

Objective To investigate the expression levels and significance of serum interleukin(IL)-23 and IL-17 in rats with nerve root injury caused by non-compressive herniated nucleus pulposus.Methods Forty-eight male SD rats were randomly divided into experimental group and control group,with 24 rats in each group.The rat model of non-compressive herniated nucleus pulposus was established in the experimental group.One,three and five weeks after modeling,eight rats in each group were randomly selected to measure the withdrawal threshold of right hind limb pain as well as serum IL-17 and IL-23 levels,and the morphological changes in lumbar nerve root tissues were observed.Results One and three weeks after operation,the experimental group exhibited lower withdrawal threshold of right hind limb pain,and higher serum IL-23 and IL-17 levels than the control group(all P<0.05).However,five weeks after operation,no statistically significant difference was found in withdrawal threshold of right hind limb pain,or serum IL-23 or IL-17 level between the two groups(all P>0.05).The results of hematoxylin-eosin staining showed that,in the control group,postoperative rats presented regular arrangement of lumbar nerve fibers with basically similar sizes,harboring red intact myelin sheath and around the axons,and no degenerative changes or inflammatory cell infiltration were found;in the experimental group,rats in week 1 postoperatively presented nerve fibers with partial disintegration of myelin sheath visible on the longitudinal section of lumbar nerve roots,harboring vacuolar lesions and inflammatory cell infiltration,nerve root injury was more severe in week 3 postoperatively,and nerve roots basically returned recovered to normal in week 5 postoperatively.Conclusion Serum IL-17 and IL-23 expression levels are higher in rats with nerve root injury caused by non-compressive herniated nucleus pulposus,and IL-23/IL-17 inflammatory axis may play a key role in the pathogenesis of radicular nerve root pain.