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Dietary emu oil supplementation suppresses 5-fluorouracil chemotherapy-induced inflammation, osteoclast formation, and bone loss

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dc.contributor.authorRaghu Nadhanan, R.
dc.contributor.authorMashtoub, S.
dc.contributor.authorSu, Y.
dc.contributor.authorScherer, M.
dc.contributor.authorHowarth, G.
dc.contributor.authorXian, C.
dc.date.issued2012
dc.description.abstractCancer chemotherapy can cause osteopenia or osteoporosis, and yet the underlying mechanisms remain unclear, and currently, no preventative treatments are available. This study investigated damaging effects of 5-fluorouracil (5-FU) on histological, cellular, and molecular changes in the tibial metaphysis and potential protective benefits of emu oil (EO), which is known to possess a potent anti-inflammatory property. Female dark agouti rats were gavaged orally with EO or water (1 ml•day_1•rat_1) for 1 wk before a single ip injection of 5-FU (150 mg/kg) or saline (Sal) was given. The treatment groups were H2O + Sal, H2O + 5-FU, EO + 5-FU, and EO + Sal. Oral gavage was given throughout the whole period up to 1 day before euthanasia (days 3, 4, and 5 post-5-FU). Histological analysis showed that H2O + 5-FU significantly reduced heights of primary spongiosa on days 3 and 5 and trabecular bone volume of secondary spongiosa on days 3 and 4. It reduced density of osteoblasts slightly and caused an increase in the density of osteoclasts on trabecular bone surface on day 4. EO supplementation prevented reduction of osteoblasts and induction of osteoclasts and bone loss caused by 5-FU. Gene expression studies confirmed an inhibitory effect of EO on osteoclasts since it suppressed 5-FU-induced expression of proinflammatory and osteoclastogenic cytokine TNFa, osteoclast marker receptor activator of nuclear factor- _B, and osteoclast-associated receptor. Therefore, this study demonstrated that EO can counter 5-FU chemotherapy-induced inflammation in bone, preserve osteoblasts, suppress osteoclast formation, and potentially be useful in preventing 5-FU chemotherapy-induced bone loss.
dc.description.statementofresponsibilityRethi Raghu Nadhanan, Suzanne M. Abimosleh, Yu-Wen Su, Michaela A. Scherer, Gordon S. Howarth and Cory J. Xian
dc.identifier.citationAmerican Journal of Physiology - Endocrinology and Metabolism, 2012; 302(11):E1440-E1449
dc.identifier.doi10.1152/ajpendo.00587.2011
dc.identifier.issn0193-1849
dc.identifier.issn1522-1555
dc.identifier.orcidMashtoub, S. [0000-0001-7308-8371]
dc.identifier.orcidScherer, M. [0000-0001-7867-6498]
dc.identifier.orcidHowarth, G. [0000-0001-6979-6084]
dc.identifier.orcidXian, C. [0000-0002-8467-2845]
dc.identifier.urihttp://hdl.handle.net/2440/72733
dc.language.isoen
dc.publisherAmer Physiological Soc
dc.relation.grantARC
dc.rightsCopyright © 2012 the American Physiological Society
dc.source.urihttps://doi.org/10.1152/ajpendo.00587.2011
dc.subjectReceptor activator of nuclear factor-kB ligand
dc.subjecttumor necrosis factor-a
dc.subjectanti-inflammatory
dc.titleDietary emu oil supplementation suppresses 5-fluorouracil chemotherapy-induced inflammation, osteoclast formation, and bone loss
dc.typeJournal article
pubs.publication-statusPublished

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