Emu Oil for Chemotherapy

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

Raghu Nadhanan R, Abimosleh SM, Su YW, Scherer MA, Howarth GS, Xian CJ.
Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia.

Abstract

Cancer 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 H(2)O + Sal, H(2)O + 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 H(2)O + 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 TNFα, osteoclast marker receptor activator of nuclear factor-κB, 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.

鸸鹋油用于化疗

膳食鸸鹋油补抑制 5-氟尿嘧啶化疗所致的炎症反应、

破骨细胞形成和骨丢失。

拉库 Nadhanan R, SM Abimosleh, 苏 YW, 谢马, 沃斯 GS, 宪  CJ.
南澳大利亚阿德莱德大学桑瑟姆健康研究所，SA 5001，澳大利亚。

摘   要

癌症化疗可引起骨量减少或骨质疏松，但潜在的机制仍不清楚，并且目前没有有效的预防性治疗措施。此项研究调查了5-氟尿嘧啶（5-FU）对胫骨干骺端组织、细胞和分子变化的损害结果，以及鸸鹋油（EO）潜在的保护作用，这是因为众所周知，鸸鹋油具有有效的抗炎特性。给雌性黑刺大豚鼠注射5-FU（150毫克/公斤）或生理盐水（SAL）的一周前，灌胃口服EO或水（1毫升•天（1）•鼠（1））。治疗组H（2）O +生理盐水，H（2）O +5氟尿嘧啶，EO + 5-FU和EO + 生理盐水。灌胃贯穿整个周期直到安乐死的前一天。（3天，4天和5天后）。组织学分析表明，在3到5天，H（2）O +氟尿嘧啶显著降低初级松质骨的高度，并且在3到4天减少次级小梁松质骨体积，这会降低成骨细胞细胞密度，同时在4天里造成骨小梁表面破骨细胞密度轻微增加。补充EO可以防止成骨细胞降低，并且防止5-FU诱发的破骨细胞和骨丢失。基因表达的研究证实鸸鹋油对破骨细胞抑制作用。这是由于EO抑制5-FU诱导的炎症和骨细胞因子TNFα；细胞核因子-κB的破骨细胞的标记受体催化剂；以及破骨细胞相关受体。

    因此，这项研究表明，EO可以对抗5-FU化疗引起的骨炎症，保护成骨细胞，抑制破骨细胞的形成，并可能在预防5-FU化疗引起的骨丢失方面有效。