Format

Send to

Choose Destination
J Bone Miner Metab. 2012 Sep;30(5):509-16. doi: 10.1007/s00774-012-0350-8. Epub 2012 Mar 13.

Poncirin prevents bone loss in glucocorticoid-induced osteoporosis in vivo and in vitro.

Author information

1
Department of Endocrinology and Metabolism, Ajou University School of Medicine, San 5, Wonchon-Dong, Yeongtong-Gu, Suwon, Gyeonggi, 443-721, South Korea.

Abstract

Poncirin, a flavonoid isolated from the fruit of Poncirus trifoliata, possesses anti-bacterial and anti-inflammatory activities. However, the action of poncirin in bone biology is unclear. In this study, the in vivo and in vitro effects of poncirin in a glucocorticoid-induced osteoporosis (GIO) mouse model were investigated. Seven-month-old male mice were assigned to the following five groups: (1) sham-implantation (sham), (2) prednisolone 2.1 mg/kg/day (GC), (3) GC treated with 10 mg/kg/day of genistein, (4) GC treated with 3 mg/kg/day of poncirin, (5) and GC treated with 10 mg/kg/day of strontium (GC + SrCl(2)). After 8 weeks, bone loss was measured by microcomputed tomography. Osteocalcin (OC) and C-terminal telopeptides of type I collagen (CTX) were evaluated in sera. Runx2 protein, OC and osteoprotegerin (OPG) mRNA expression, alkaline phosphatase (ALP) activity, and mineral nodule assay were performed in C3H10T1/2 or primary bone marrow stromal cells. Poncirin significantly increased the bone mineral density and improved the microarchitecture. Poncirin increased serum OC, Runx2 protein production, expression of OC and OPG mRNA, ALP activity, and mineral nodule formation; and decreased serum CTX. These effects were more prominent in the poncirin group compared to the other positive control groups (genistein and strontium). The poncirin-mediated restoration of biochemical bone markers, increased bone mineral density, and improved trabecular microarchitecture likely reflect increased bone formation and decreased bone resorption in GIO mice.

PMID:
22407507
DOI:
10.1007/s00774-012-0350-8
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center