Effect of isopsoralen on Smad7 in osteoblastic MC3T3-E1 cells

Abstract

The primary pathological change in postmenopausal osteoporosis (PM-OP) is bone collagen loss caused by estrogen depletion. Osteoblasts synthesize type I collagen, which composes the organic matrix of bone. Although isopsoralen stimulates osteoblastic cell proliferation and differentiation, transforming growth factor (TGF)-β1 is an important cell signaling factor for stimulating collagen synthesis. To explore the association between isopsoralen and the synthesis of collagen in vitro, the molecular and biological association between isopsoralen and TGF-β signaling was examined. (CAGA) 12-luciferase-reporter gene was used to measure TGF-β1 signaling activity. Type I collagen was detected by semiquantitative reverse transcription polymerase chain reaction, and mothers against decapentaplegic homolog 7 (Smad7) protein expression levels were analyzed by western blotting. The expression of collagen in MC3T3-E1 cells stimulated with isopsoralen was significantly upregulated compared with the control groups (P<0.05). Conversely, isopsoralen significantly decreased Smad7 protein expression compared with the control groups (P<0.05). Moreover, it was observed that isopsoralen activates the TGF-β1 signaling pathway and ultimately promotes collagen synthesis through inhibition of Smad7 protein expression. Therefore, isopsoralen is a potential target for the treatment of PM-OP.