Bilobalide Alleviates Il-17-Induced Inflammatory Injury In Atdc5 Cells By Downregulation Of Microrna-125a

Ankylosing spondylitis (AS) is a high disability and greatly destructive disease. In this study, we preliminarily studied the function and mechanism of bilobalide (BIL) on interleukin (IL)-17-induced inflammatory injury in ATDC5 cells. CCK-8 and migration assays were used to detect the functions of IL-7, BIL, and microRNA (miR)-125a on cell viability and migration. The miR-125a level was changed by transfection, and tested by real-time quantitative polymerase chain reaction. Additionally, Western blot tested the levels of inflammatory factors (IL-6 and tumor necrosis factor-alpha), matrix metalloproteinases (MMPs), and pathway-related proteins. Moreover, the enzyme-linked immunosorbent assay also was used to detect inflammatory factor levels. IL-7 was used to construct an inflammatory injury model in ATDC5 cells. Based on this, BIL inhibited IL-17-induced cell viability, migration, and expressions of inflammatory factors and MMPs. Furthermore, we found BIL negatively regulated miR-125a, and the miR-125a mimic could partly reverse the effects of BIL on IL-17-injury. Finally, we showed that BIL inhibited the c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NF-kappa B) pathways, and the miR-125a mimic had the opposite effect. BIL inhibited IL-17-induced inflammatory injury in ATDC5 cells by downregulation of miR-125a via JNK and NF-kappa B signaling pathways.