Volume 29, Issue 3
DOI: 10.24205/03276716.2020.935
Effect of Ibandronate On MAPK Pathway and Autophagy in Osteoporosis
Abstract
Aim: To investigate the role of ibandronate in osteoporosis (OP) and its association with mitogen-activated protein kinase (MAPK) pathway.
Methods: MC3T3-E1 cells were assigned into control group (CG), model group (MG) and intervention group (IG). The MG and IG were treated with dexamethasone (DEX) to establish cell models of OP, and IG was treated with ibandronate additionally. Cell apoptosis and viability were tested with flow cytometry and, cell counting kit-8 (CCK-8) respectively. Western Blotting (WB) was employed to quantify receptor activator of NF-κB ligand (RANKL), osteoprotegerin (OPG), P38MAPK, phosphorylated-P38MAPK (p-
P38MAPK), Beclin-1 and light chain 3-II (LC3-II).
Results: MG presented remarkably decreased cell viability and protein levels of OPG, pP38MAPK, Beclin-1, LC3-II than CG, as well as increased apoptosis and RANKL. Whereas results were quite the opposite in IG: Cell viability and protein levels of OPG, p-P38MAPK, Beclin-1, LC3-II in IG were remarkably higher, and the apoptosis and RANKL were remarkably lower than those in MG.
Conclusion: Ibandronate enhances the viability and inhibits the apoptosis of osteoblasts by activating the phosphorylation of P38MAPK and upregulating autophagy, thereby relieving OP.
Keywords
ibandronate; osteoporosis; MAPK pathway; autophagy