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Conclusion In conclusion, we established the healing effects of IGF-1 in chondrocytes and a rabbit model against osteoarthritis. IGF-1 inhibited the NF-κB, p38 (MAPK), and PI3K/AKT signaling pathways, thereby preventing MMPs expression during OA pathogen, and also balanced collagen type II and proteoglycan and formation of hyaline cartilage. Therefore, in articular cartilage lesions, Intra-articular injection of IGF-1 leading a better tactic for effective and efficient therapy. So, our study revealed that IGF-1 could be a potential therapeutic mediator for the management of cartilage damage related to OA. However, our initial finding only on animal and cell levels of anti-OA, further needed to clinical implementation evaluation.

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