A Novel RANKL-Targeted Furoquinoline Alkaloid Ameliorates Bone Loss in Ovariectomized Osteoporosis through Inhibiting the NF-κB Signal Pathway and Reducing Reactive Oxygen Species

Figure 4

DIC abrogates NFATc1 and CTSK expression, which is further related to specific osteoclastogenesis genes, and inhibits the NF-κB/IκBα pathway (a). Expression of specific genes during osteoclast differentiation. DIC suppresses the mRNA levels of CTSK, MMP9, RANKL, and NFATc1 (b). Representative images show the inhibitory effects of DIC on NFATc1, CTSK, and c-Fos (c). Quantification of the band intensity ratios of NFATc1, CTSK, and c-Fos relative to β-actin (d). Western blotting was used to analyze the primary antibodies against NF-κB p65/p-p65/IκBα. The images show that DIC inhibited the NF-κB pathway and promoted IκBα downstream (e). Quantitative analyses of p-p65 were normalized to total p65. The phosphorylation levels of NF-κB p65/p-p65/IκBα were significantly suppressed by DIC from 20 minutes to 60 minutes. All bar charts are presented as the ; . , relative to the nontreatment group. , relative to the RANKL treatment group.

(a)

(b)

(c)

(d)

(e)