Abstract Title:

Arctigenin promotes bone formation involving PI3K/Akt/PPARγ signaling pathway.

Abstract Source:

Chem Biol Drug Des. 2019 Dec 28. Epub 2019 Dec 28. PMID: 31883507

Abstract Author(s):

Hongbo Li, Chunli Yang, Min Lan, Xingen Liao, Zhiming Tang

Article Affiliation:

Hongbo Li


This study investigated the mechanisms through which arctigenin promotes osteogenesis. Bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (OVX) rats were differentiated into osteoblasts, and osteogenesis was evaluated via Alizarin Red S (ARS) staining and alkaline phosphatase (ALP) measurements in cultured BMSCs. The levels of phosphorylated AKT serine/threonine kinase 1 (p-Akt), and peroxisome proliferator-activated receptor gamma (PPARγ) expression were quantified by western blot analysis. The levels of urine calcium (U-Ca), urine phosphorus (U-P), serum ALP, and bone mineral density (BMD) of OVX rats were assessed in vivo. The results showed that treatment with arctigenin in rat BMSCs enhanced mineralization, increased ALP activity, increased the expression of Akt and p-Akt, and decreased PPAR γ expression, consistent with its ability to promote osteoblast differentiation. Furthermore, arctigenin prevented OVX-induced osteoporosis in rats by increasing BMD and ALP activity and inhibiting the loss of Ca and P. In contrast, treatment with LY294002, a selective inhibitor of the phosphatidylinositol 3-kinase (PI3K), produced the opposite phenotype. These data suggest that the protective effects of arctigenin on BMSCs and OVX rat models result from the induction of osteogenesis involving the PI3K/Akt/PPAR γ axis.

Study Type : Animal Study
Additional Links
Pharmacological Actions : Osteoprotective : CK(971) : AC(351)

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