ABSTRACT
OBJECTIVES@#Chondrocyte apoptosis is an important process in the pathogenesis of osteoarthritis. Mangiferin exerts multiple pharmacological effects such as anti-inflammatory and anti-apoptosis. However, the role of mangiferin in chondrocyte apoptosis is not clear. In this study, we aimed to explore the role of mangiferin in IL-1β-induced chondrocyte apoptosis.@*METHODS@#ATDC5 cells were randomly divided into a control group, a IL-1β group, a MFN-L group, a MFN-M group, a MFN-H group and a MFN+LY294002 group. Cells in the control group were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN-L group, the MFN-M group and the MFN-H group were pretreated with 5, 10 and 20 μmol/L mangiferin for 1 h respectively, and then they were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN+LY294002 group were treated with LY294002 (25 μmol/L) for 1 h, then mangiferin (20 μmol/L) and IL-1β (10 ng/mL) for 1 h and 24 h, respectively. Cell viability was detected by CCK-8 assay and cell apoptosis was measured by flow cytometry. Colorimetric assay was conducted to measure the caspase-3 activity. The protein levels of Bcl-2, Bax, and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway related proteins were detected by Western blotting.@*RESULTS@#Compared to the control group, cell viability was significantly decreased; cell apoptosis, caspase-3 activity and Bax protein expression were significantly increased; the protein levels of Bcl-2, p-PI3K, and p-Akt were significantly decreased in the IL-1β group (all @*CONCLUSIONS@#Mangiferin could attenuate IL-1β-induced apoptosis of the mice chondrocytes, which is mediated by the activation of PI3K/Akt signaling pathway.
Subject(s)
Animals , Mice , Apoptosis , Chondrocytes , Interleukin-1beta , Phosphatidylinositol 3-Kinases , Proto-Oncogene Proteins c-akt , XanthonesABSTRACT
AIM: To investigate whether salidroside has influence on the activities of endothelial progenitor cells (EPCs) and its mechanism.METHODS:Mononuclear cells from normal human peripheral blood were cultured in fi-bronectin coated flasks in endothelial progenitor medium .After 7 d, EPCs were characterized as adherent cells with acLDL-DiI uptaking and lectin binding by direct fluorescent staining .The proliferation and migration of EPCs were analyzed by MTT assay and Transwell chamber assay , respectively.The EPCs adhesion assay was performed by re-plating the cells on fibronectin-coated dishes , and then adherent cells were counted .NO and Akt protein were also detected .RESULTS:Sali-droside promoted EPCs proliferative , migratory and adhesive capacities in a concentration dependent manner .Salidroside also increased NO secretion , and the level of phosphorylated Akt protein .However , the effects of salidroside on EPCs were inhibited by phosphoinositide 3-kinase inhibitor LY294002.CONCLUSION:Salidroside regulates the activity of EPCs by phosphoinositide 3-kinase/Akt signaling pathway .
ABSTRACT
@#Osteotendinous junction (OTJ) is the main structure of tendinopathy. Cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) and phosphoinositide-3 kinase (PI3K)/Akt is active under the stress, and expresses in OTJ. This article summarized the role of these two signaling pathways in OTJ.