Pantoprazole (PPZ) Inhibits RANKL-Induced Osteoclast Formation and Function In Vitro and Prevents Lipopolysaccharide- (LPS-) Induced Inflammatory Calvarial Bone Loss In Vivo

Figure 1

PPZ inhibits RANKL-induced osteoclast (OC) formation and suppresses RANKL-induced OC-related gene expression in vitro. (a) Chemical structure of PPZ. (b, c) Effects of PPZ on viability and proliferation of bone marrow-derived macrophages (BMMs) at 48 and 72 hrs, respectively. The absorbance of the optical density was measured at 570 nm (OD570). (d) Quantitative analysis of the numbers of TRAP-positive multinucleated () cells formed in the presence of different concentrations of PPZ. (e) BMMs were cultured under RANKL stimulation with 0, 3, 6, 12.5, and 25 μM of PPZ for 7 days and treated with TRAP staining (magnification: 100x; ). TRAP-positive cells with ≥3 nuclei were considered OCs (magnification: 100x; ). (f–h) Quantitative real-time PCR analyses of relative levels of OC marker genes (TRAP, CTSK, and V-ATPase d2) at day 0, day 2, and day 4 in the presence of PPZ (12.5 μM). The expression levels of these genes were normalized to the expression of β-actin. Data are presented as ; , relative to RANKL-induced controls.

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