JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Add like
Add dislike
Add to saved papers

Osteogenic activity of silymarin through enhancement of alkaline phosphatase and osteocalcin in osteoblasts and tibia-fractured mice.

Bone-remodeling imbalance induced by increased bone resorption and osteoclast formation is known to cause skeletal diseases such as osteoporosis. There has been growing interest in the anabolic natural agents that enhance bone formation. Silymarin is flavonolignans extracted from blessed milk thistle. Several studies suggest that silymarin possesses antihepatotoxic properties and anticancer effects against carcinoma cells. This study investigated promoting effects of silymarin on differentiation and mineralization of osteoblastic MC3T3-E1 mouse cells and on bone mineral density (BMD) by in vivo fracture experiments. Osteoblasts were treated with 1-20 μmol/L silymarin for 15 days in a differentiating medium. In addition, this study explored signaling pathways implicated in the osteoblastogenesis of silymarin. It was found that silymarin stimulated alkaline phosphatase (ALP) activity and calcium nodule formation in a dose-dependent manner with a substantial effect on osteoblast proliferation. Silymarin treatment enhanced collagen secretion, osteocalcin transcription and bone morphogenetic protein (BMP) expression. The BMP inhibitor noggin suppressed the silymarin-promoted ALP activity in differentiated osteoblasts, suggesting that its osteoblastogenic actions entail the BMP pathway. This was proved by increased SMAD1/5/8 phosphorylation and runt-related transcription factor 2 (Runx2) expression in the presence of silymarin. In 21-day fracture-healing experiments, fractured and silymarin (10 mg/kg)-treated C57BL/6 mice showed better bone healing than fractured mice. Silymarin supplementation improved tibial bone strength with elevated BMD and serum levels of osteogenic ALP and osteocalcin. Taken together, these results demonstrate, for the first time, that silymarin has a potential to enhance osteoblastogenesis through accelerating BMP/SMAD/Runx2 signal pathways and to improve fracture healing and bone strength in mouse tibiae.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app