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Caffeic acid phenethyl ester protects against glucocorticoid-induced osteoporosis in vivo : Impact on oxidative stress and RANKL/OPG signals
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt; Chapman University, Irvine, CA, USA.
Sharjah Institute for Medical Research, University of Sharjah, Sharjah, United Arab Emirates; Department of Medical Biochemistry, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.ORCID iD: 0000-0001-5394-9082
Sharjah Institute for Medical Research, University of Sharjah, Sharjah, United Arab Emirates; Department of Pharmacology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt.
2017 (English)In: Toxicology and Applied Pharmacology, ISSN 0041-008X, E-ISSN 1096-0333, Vol. 324, p. 26-35Article in journal (Refereed) Published
Abstract [en]

Glucocorticoid-induced osteoporosis (GIO) is one of the most common causes of secondary osteoporosis. Given that glucocorticoids are considered as a main component of the treatment protocols for a variety of inflammation and immune-mediated diseases besides its use as adjuvant to several chemotherapeutic agents, it is crucial to find ways to overcome this critical adverse effect. Caffeic acid phenethyl ester (CAPE), which is a natural compound derived from honeybee propolis displayed promising antiosteoporotic effects against mechanical bone injury in various studies. The current work aimed at investigating the potential protective effect of CAPE against GIO in vivo with emphasis on the modulation of oxidative status and receptor activator of NF-kB ligand (RANKL)/osteoprotegrin (OPG) signaling. The results showed that CAPE opposed dexamethasone (DEX)-mediated alterations in bone histology and tartarate-resistant acid phosphatase (TRAP) activity. In addition, CAPE restored oxidative balance, Runt-related transcription factor 2 (RunX2) expression and reduced caspase-3 activity in femur tissues. Co-administration of CAPE with DEX normalized RANKL/OPG ratio and Akt activation indicating a reduction in DEX-osteoclastogenesis. In conclusion, concurrent treatment of CAPE with DEX exhibited promising effects in the protection against DEX-induced osteoporosis through opposing osteoclastogenesis and protecting osteoblasts. The potent antioxidant activity of CAPE is, at least in part, involved in its anti-apoptotic effects and modulation of RunX2 and RANKL/OPG signals. The use of CAPE-enriched propolis formulas is strongly recommended for patients on chronic glucocorticoid therapy to help in the attenuation of GIO.

Place, publisher, year, edition, pages
Maryland Heights, MO, United States: Elsevier, 2017. Vol. 324, p. 26-35
Keywords [en]
Dexamethasone; Caffeic acid phenethyl ester; Osteoporosis; GSH; SOD; Apoptosis
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:liu:diva-184319DOI: 10.1016/j.taap.2017.03.021ISI: 000400416500003PubMedID: 28363435Scopus ID: 2-s2.0-85016620129OAI: oai:DiVA.org:liu-184319DiVA, id: diva2:1651519
Note

Funding: MFT is supported by a Fulbright Scholarship FY2015/2016.

Available from: 2022-04-12 Created: 2022-04-12 Last updated: 2022-04-21Bibliographically approved

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El-Serafi, Ahmed Taher

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