Resveratrol prevents osteoporosis in ovariectomized rats by regulating microRNA-338-3p
Osteoporosis is a disease characterized by loss of bone mass and degeneration of the microstructure of bone. Resveratrol (3,5,4trihydroxystilbene; RESV) may delay the onset of a variety of agerelated diseases. In the present study, an ovariectomized female rat model was used to detect the changes in microRNAs (miRNAs/miRs) following RESV treatment. Subsequently, the target genes of miRNA were predicted using TargetScan software and determined using a dualluciferase reporter assay. Finally, the role of miR3383p in the proliferation and differentiation of human osteoblast (HOB) cells was confirmed. The predominant finding of the present study was the identification of an intact mechanism of the effect of RESV in osteoporosis treatment. The results suggested that RESV suppresses miR3383p, followed by an increase in the expression of runtrelated transcription factor 2 in HOB cells.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
Document Type: Research Article
Affiliations: Department of Orthopaedics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China
Publication date: August 1, 2015
More about this publication?
- Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
- Editorial Board
- Information for Authors
- Submit a Paper
- Subscribe to this Title
- Information for Advertisers
- Terms & Conditions
- Ingenta Connect is not responsible for the content or availability of external websites