目的:研究川芎嗪对白介素-1β(IL-1β)诱导退变的终板软骨细胞的影响。方法:体外分离培养大鼠椎间盘终板软骨细胞,并用IL-1β和川芎嗪处理,进行细胞增殖、细胞免疫化学染色和RT-PCR检测。结果:川芎嗪(6.25-25.00μmol/L)逆转IL-1β对大鼠终板软骨细胞增殖的抑制影响,抑制IL-1β诱导的软骨细胞IL-1β、肿瘤坏死因子-α(TNF-α)、环氧化酶-2(COX-2)和诱导型一氧化氮合酶(i NOS m RNA)过量表达,逆转IL-1β对于Col2-1、Aggrecan、MMP-13和ADAMTS-5 m RNA表达的影响,增加IL-1β诱导后Ⅱ型胶原的蛋白表达。结论:本研究证实川芎嗪可以抑制IL-1β诱导后软骨细胞的退变表现。
Rheumatoid arthritis （RA） and osteoarthritis （OA） are the two most common joint diseases, and they have characterization of synovial inflammation and cartilage destruction, associated with the accumulation of numerous catabolic mediators and inflammatory cells in the synovial space and surrounding soft tissues. How these factors are cleared and if the ＂clearance＂ process contributes to pathogenesis of arthritis are not known. Recently, we found the existence of the peri-articular lymphatic system in mouse joints. The blockade of lymphangiogenesis and lymphatic draining function accelerates while stimulation of lymphatic function attenuates the severity of joint tissue lesions in mouse models of RA and OA. More importantly, we noticed the similarity between the dysfunction of lymphatic drainage in arthritic joints and ＂Bi＂ theory of Chinese medicine （CM）, and demonstrated that several Bi disease-treated herbal drugs directly affect the function of lymphatic endothelial cells. Here we review the advances about the interactions between joint inflammation and changes in the peri-articular lymphatic system and discuss our view of linking ＂Bi＂ theory of CM to lymphatic dysfunction in arthritis.
