The Inflammatory Mechanism of Osteoarthritis
學生姓名:
龍秉廷
指導教授:
龔瑞林
學 號:
10332017
學期:
103下
摘 要:
Osteoarthritis (OA), which is a chronic degenerative joint disorder that causes joint pain and dysfunction, is characterized by progressive structural changes in articular cartilage, persistent loss of tissue cellularity, and degeneration of the extracellular matrix (ECM). The aim of this study was to explore how to stimulate IL-1b on MMP-13 cause cartilage cell damage. First the study evaluated the effects of this study was to determine how PI-3 kinase-Akt signaling regulates these seemingly opposing functions. The results showed that chondrocyte integrates signals from the PI-3 kinase-Akt pathway with signals from MAP kinases and the JAK-STAT pathway to allow for a differential response to a pro-anabolic (IGF-1) and a pro-catabolic (IL-1 plus OSM) stimulus. Secondly, even though increasing evidences on miRNA involvement in human pathological responses, the distinct roles and related mechanisms of miRNAs in the pathology of OA are not yet fully understood. This suggests that miR-222 may serve as a potential HDAC-4 inhibitor for the therapeutic control of OA. Thirdly, berberine, a plant alkaloid used in Chinese medicine, has broad cell-protective functions in a variety of cell lines. Chondrocyte apoptosis contributes to the pathogenesis of cartilage degeneration in OA. The resultant chondroprotective effects indicate that berberine merits consideration as a therapeutic agent in OA. In conclusion,
10332017-2-龍秉廷-龔瑞林.pdf