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Mechanisms by which electroacupuncture-mediated histone acetylation mitigates bone loss in rats with ovariectomy-induced osteoporosis

The aim of the present study was to investigate the effectiveness of electroacupuncture (EA) on ovariectomy-induced osteoporotic rats to elucidate potential mechanisms by which EA regulates acetylation of histones in caput femoris. A total of 40 female Sprague-Dawley rats were randomly allocated int...

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Detalles Bibliográficos
Autores principales: Shu, Qing, Shao, Yuwei, Liu, Ruolan, Hu, Yan, Peng, Zhao, Tian, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453644/
https://www.ncbi.nlm.nih.gov/pubmed/32945471
http://dx.doi.org/10.3892/mmr.2020.11430
Descripción
Sumario:The aim of the present study was to investigate the effectiveness of electroacupuncture (EA) on ovariectomy-induced osteoporotic rats to elucidate potential mechanisms by which EA regulates acetylation of histones in caput femoris. A total of 40 female Sprague-Dawley rats were randomly allocated into four groups: Sham operation, ovariectomy-induced osteoporosis (OVX), EA and 17β-estradiol (E2) treatments. After 8 weeks of intervention, the trabecular morphology of each group was measured by micro-computed tomography. Biomarkers of bone metabolism in serum were detected. The protein expression of histone deacetylase 2 (HDAC2), histone H3, Ac-histone H3 and downstream cytokines involved in osteoblast and osteoclast differentiation were detected. The results showed that EA and E2 both prevented bone loss and improved trabecular morphology in OVX rats. EA was found to suppress the protein expression of HDAC2 and promoted the acetylation of histone H3 compared with the OVX model group. The results indicated that EA promoted the differentiation of osteoblasts, and suppressed that of osteoclasts, thereby improving the trabecular morphology. E2 was shown to regulate the expression of runt-related transcription factor 2 and receptor activator of nuclear factor-κB ligand without modulating the expression of HDAC2, and therefore diverged mechanistically from EA. Overall, the results of the present study suggested that the mechanisms through which EA improved bone mineral density and trabecular morphology may involve the modulation of histone H3 acetylation and regulation of osteoblast and osteoclast differentiation.