Hesperidin Ameliorates Dexamethasone-Induced Osteoporosis by Inhibiting p53

Abstract

Osteoporosis is one of the most frequent skeletal disorders and a major cause of morbidity and mortality in the expanding aging population. Evidence suggests that hesperidin may have a therapeutic impact on osteoporosis. Nevertheless, little is known about the role of hesperidin in the development of osteoporosis. Bioinformatics analyses were carried out to explore the functions and possible molecular mechanisms by which hesperidin regulates osteogenic differentiation. In the present study, we screened and harvested 12 KEGG pathways that were shared by hesperidin-targeted genes and osteoporosis. The p53 signaling pathway was considered to be a key mechanism. Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.

Analyses of Physical and Chemical Compositions of Different Medicinal Specifications of CRPV by Use of Multiple Instrumental Techniques Combined with Multivariate Statistical Analysis

“…It not only has a potential therapeutic effect on Alzheimer’s disease, but may also reduce alcohol-induced liver damage [ 24 , 25 ]. Hesperidin has not only reduced in vivo lipid accumulation, indicating its potential anti-hyperlipidemic effects, but also has anti-osteoporotic effects [ 26 , 27 ].…”