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Aim To observe whether paeonol can in-hibit fibronectin (FN) and intercellular cell adhension molecule-1 (ICAM-1) expressions in high glucose (HG)-induced glomerular mesangial cells(GMCs) via up-regulating CKIP-1 and activating the Nrf2 signaling pathway. Methods The effects of paeonol on the ex-pressions of CKIP-1,Nrf2,FN and ICAM-1 were eval-uated in GMCs treated with HG. Small interfering RNA was used to deplete CKIP-1 protein expression, and Western bolt was used to detect the expressions of Nrf2, HO-1 and SOD1. DHE fluorescent probe tech-nique was used to determine intracellular superoxide level. Results The protein levels of CKIP-1 and Nrf2 were elevated by paeonol in HG-treated GMCs. In the meanwhile,the expressions of Nrf2 downstream antiox-idant enzymes, i.e. HO-1 and SOD1, were also up-regulated by paeonol, which was accompanied by re-ductions of superoxide and H2O2levels. Importantly, paeonol reversed the excessive accumulation of FN and ICAM-1 in HG-induced GMCs. si-CKIP-1 decreased the up-regulation of Nrf2,HO-1 and SOD1 expressions during paeonol treatment, which was accompanied by increased superoxide and H2O2levels. Furthermore, si-CKIP-1 reversed the down-regulated levels of FN and ICAM-1 induced by paeonol. Conclusion Pae-onol inhibits the expressions of FN and ICAM-1 in HG-treated GMCs possibly by up-regulating CKIP-1 and activating the Nrf2 signaling pathway.
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Objective:To investigate the regulation of proliferation and differentiation of bone marrow mesenchymal stem cells(BM-SCs)by CKIP-1 in vitro.Methods:BMSCs from CKIP-1 nock out(KO)and wild type(WT)C57 mice were isolated and cultured u-sing adherence method in vitro.BMSCs of the 3rd passage were induced to osteogenic and adipgenic differentiation.Cell proliferation was examined by MTT assay.Cell surface markers were tested by FCM.The osteogenic and adipogenic differentiation was studied by alkaline phosphatase (ALP)staining,alizarin red staining and oil red O staining.Results:The proliferation and cell marke expression of the 2 groups were similar.ALP staining of KO group was strong than that of WT group after osteogenic induction.Alizarin red stai-ning showed that there were more mineralized nodules in BMSCs of KO group than in those of WT group.Oil red O staining of KO mice BMSCs was stronger than that of WT.Conclusion:CKIP-1 deficiency can enhance the osteogenic and adipogenic differentiation without influence on the proliferation of BMSCs.
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Osteoporosis (OP) is one of the bone metabolic diseases which seriously harms the health and lives of people. The main cause of OP is that the balance between bone formation and bone absorption, i.e. the balance of the bone remodeling process,is no longer exist. When the bone absorption dominates the process, it will lead to osteopenia, destruction of bone microstructure and increased rate of fracture. Previous studies have shown that casein kinase 2-interacting protein-1 (CKIP-1) plays an important role in the process of bone tissue proliferation and differentiation. It mainly interacts with Smad ubiquitination regulatory factor 1 (Smurf 1) to affect bone metabolism. This review analyzes and summarizes the impact of CKIP-1 on bone tissue osteogenic differentiation direction and its mechanism, which may provide new idea and research orientation for future clinical treatment of osteoporosis.