灯盏花素对大鼠膝骨关节炎膝关节软骨的影响

Effect of Breviscapine on Knee Joint Cartilage in Rats with Knee Osteoarthritis

目的探讨灯盏花素(breviscapine,BE)对膝骨关节炎(osteoarthritis,OA)模型大鼠关节软骨的影响。方法通过内侧半月板失稳(destabilization of the medial meniscus,DMM)诱导OA大鼠模型,BE和塞来昔布(celecoxib,Cel)分别通过灌胃向大鼠给药。通过苏木精-伊红(hematoxylin&eosin,HE)染色观察大鼠骨关节炎软骨损伤和细胞浸润情况,番红O-固绿染色观察软骨损伤情况,甲苯胺蓝染色观察软骨损伤,免疫组织化学(Immunohistochemistry,IHC)染色观察软骨组织中collagen-Ⅱ和p-JNK阳性细胞比例,酶联免疫吸附(enzyme linked immunosorbent assay,ELISA)试剂盒检测大鼠血清中炎性细胞因子IL-1β、TNF-α和IL-6的浓度。结果OA组大鼠膝骨组织中软骨细胞层厚度较sham组变薄(P<0.0001),软骨细胞损伤加重(P<0.001),促炎细胞因子IL-1β(P<0.001)、TNF-α(P<0.001)和IL-6(P<0.001)水平与sham组相比明显升高,p-JNK阳性率升高。相比较于OA组,BE灌胃给药可缓解DMM诱导的大鼠膝骨关节的软骨损伤(P<0.05),抑制促炎细胞因子的水平(P<0.01)以及p-JNK的阳性率。结论BE可缓解DMM诱导的OA大鼠软骨损伤,抑制炎性细胞因子的生成。BE可能通过调节JNK信号通路参与OA软骨细胞损伤的调控。

Objective To explore the effect of breviscapine(BE)on articular cartilage of knee osteoarthritis(OA)in model rats.Methods The knee OA rat model was induced by destabilization of the medial meniscus(DMM),and then the rats were given BE and celecoxib(Cel)by gastric infusion,respectively.Hematoxylin&eosin(HE)staining was used to observe the cartilage injury and cell infiltration in OA rats.Saffron O-solid green staining was used to observe the cartilage injury.Toluidine blue staining was used to observe the cartilage injury.The proportion of collagen-Ⅱand p-JNK positive cells in the cartilage tissue was detected by immunohistochemistry(IHC)staining,and the concentrations of inflammatory cytokines IL-1β,TNF-αand IL-6 in the serum of rats were detected by enzyme-linked immunosorbent assay(ELISA).Results In the OA group,the thickness of the chondrocyte layer in the knee bone tissue was thinner than that in the sham group(P<0.0001),and the injury of chondrocytes was aggravated(P<0.001).Compared with the sham group,the level of proinflammatory cytokines(IL-1βTNF-αand IL-6)was significantly higher(P<0.001),and the positive rate of p-JNK was increased.Compared with the OA group,gastric infusion of BE alleviated DMM-induced cartilage injury in the knee joints of rats(P<0.05),inhibited the levels of inflammatory cytokines(P<0.01)and the positive rate of p-JNK.Conclusion BE could alleviate DMM-induced cartilage injury in OA rats and inhibit the production of inflammatory cytokines.BE might be involved in the regulation of OA chondrocyte injury by regulating the JNK signaling pathway.