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

Emu Oil Chemotherapy Scientific Publication

Abstract published in American Journal of Physiology – Endocrinology and Metabolism

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

  1. Rethi Raghu Nadhanan1,2
  2. Suzanne M Abimosleh4
  3. Yu-Wen Su1
  4. Michaela A Scherer1
  5. Gordon S Howarth3,4
  6. Cory J Xian1,2

Author Affiliations:

1Sansom Institute for Health Research, University of South Australia, Adelaide, Australia
2School of Paediatrics and Reproductive Medicine, University of Adelaide, Adelaide, Australia
3School of Animal and Veterinary Sciences, Roseworthy Campus, University of Adelaide, Adelaide, Australia
4Gastroenterology Department, Women’s and Children’s Hospital, Adelaide, Australia

  • Submitted 18 November 2011
  • Revision received 20 March 2012
  • Accepted 20 March 2012

Abstract

Cancer chemotherapy can cause osteopenia or osteoporosis; yet underlying mechanisms remains 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 orally gavaged with EO or water (1 mL/d (day)/rat) for one week before a single i.p. injection of 5-FU (150 mg/kg) or Sal (saline) 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 (d 3, d 4 and d 5 post 5-FU). Histological analysis showed that H2O+5-FU significantly reduced heights of primary spongiosa on d 3 and d 5 and trabecular bone volume of secondary spongiosa on d 3 and d 4. It slightly reduced density of osteoblasts and caused an increase in the density of osteoclasts on trabecular bone surface on d 4. EO supplementation prevented reduction of osteoblasts and induction of osteoclasts and bone loss caused by 5-FU. Gene expression studies confirmed inhibitory effect of EO on osteoclasts as it suppressed 5-FU-induced expression of proinflammatory and osteoclastogenic cytokine TNFα, osteoclast markers receptor activator of nuclear factor kappa-B (RANK) and osteoclast associated receptor (OSCAR). 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.

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