基于脊髓型颈椎病发病机制研究黄芪总苷对大鼠模型椎间盘中相关因子表达的影响

Effects of astragaloside on the expression of correlation factors in intervertebral discs of rat models based on the study of pathogenesis of cervical spondylotic myelopathy

目的探讨黄芪总苷对大鼠退变颈椎间盘内白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)含量的影响。方法将110只SD大鼠随机分为空白对照组、模型组、黄芪总苷高剂量组、黄芪总苷中剂量组、黄芪总苷低剂量组和甲钴胺对照组,每组18只(2只造模失败剔除)。造模成功后,按要求给予药物灌胃,分别于灌胃前后监测大鼠的运动功能,灌胃1,2,4周后分3次处死大鼠,取各组大鼠颈椎间盘,用放射免疫分析法分别检测标本中IL-1β,TNF-α的含量。结果与空白对照组比较,造模成功后即给药前,其他5组斜板试验角度均明显减小(P<0.05);在给药1,2,4周后,与模型组比较,黄芪总苷高、中、低剂量组,甲钴胺对照组斜板试验角度均明显增大,IL-1β,TNF-α含量均明显降低(P<0.05),且以黄芪总苷中剂量组作用最为显著(P<0.05)。结论退变椎间盘不但释放大量的细胞因子,还可加速椎间盘的退变,黄芪总苷能降低退变颈椎间盘中细胞因子的含量,具有减弱炎性反应和减缓椎间盘退变的作用,且存在量效关系。

Objective To explore the effects of astragaloside on IL-1β,TNF-α in degenerative intervertebral discs of rats. Methods 110 rats were randomly divided into control group,model group,astragaloside high-dose group,astragaloside medium-dose group,astragaloside low-dose group and mecobalamin group,18 rats in each group( 2 failures in modeling). After successful modeling,all rats were given drug intragastric administration.Motor functions were monitored before and after drug intragastric administration. On 1st,2ndand 4thweek after drug intervention,all rats were killed and cervical discs were sampled to detect the contents of IL-1β,TNF-α by radio immunoassay. Results Compared with control group,the degree of slopping plate test in other 5 groups decreased o bviously before administration( P<0.05); On 1^(st),2^(nd) and 4^(th) week after drug intervention,compared with model group,the degree of slopping plate test in astragaloside high-dose,medium-dose,low-dose group and mecobalamin group increased remarkably,the contents of IL-1β,TNF-α decreased significantly( P<0.05),and the effects of astragaloside medium-dose group were remarkable( P<0.05). Conclusion The degenerative intervertebral disc can release large number of cell factors,also accelerate the degeneration. Astragaloside can reduce the content of cell factor,also react on weakening inflammatory action and slackening the degeneration with dose-effect relationship.