Journal Article
Research Support, Non-U.S. Gov't
Add like
Add dislike
Add to saved papers

11β-hydroxysteroid dehydrogenases-2 decreases the apoptosis of MC3T3/MLO-Y4 cells induced by glucocorticoids.

The aim of the present study was to confirm the role of 11β-hydroxysteroid dehydrogenases type 2(11β-HSD-2) in steroid induced osteonecrosis of the femoral head(SANFH). We cultured mouse bone-like cells (MLO-Y4) and mouse osteoblast-like cells (MC3T3-E1). After overexpressed 11β-HSD-2 successfully, we induced cell apoptosis by dexamethasone (DXM). The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected. Then, we constructed 11β-HSD-2 siRNA plasmid and represented it on MLO-Y4/MC3T3-E1 Cells, to down-regulate the 11β-HSD-2 expression. After that, we used dexamethasone to induce cell apoptosis. The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected again. In the overexpression model of cells, we found that the amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells are lower than that of control groups. The amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells were more than before when we reduced the expression of 11β-HSD-2. In our study, we concluded that 11β-HSD-2 plays an important role in the development of bone or osteoblast cell apoptosis, and the decreased expression of 11β-HSD-2 may aggravate steroid induced bone/osteoblast cell apoptosis.

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.

Related Resources

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