Abstract
The nutritional benefits of pomegranate have attracted great scientific interest. The pomegranate, including the pomegranate peel, has been used worldwide for many years as a fruit with medicinal activity, mostly antioxidant properties. Among chronic diseases, osteoporosis, which is associated with bone remodelling impairment leading to progressive bone loss, could eventually benefit from antioxidant compounds because of the involvement of oxidative stress in the pathogenesis of osteopenia. In this study, with in vivo and ex vivo experiments, we investigated whether the consumption of pomegranate peel extract (PGPE) could limit the process of osteopenia. We demonstrated that in ovariectomized (OVX) C57BL/6J mice, PGPE consumption was able to significantly prevent the decrease in bone mineral density (−31.9%; p < 0.001 vs. OVX mice) and bone microarchitecture impairment. Moreover, the exposure of RAW264.7 cells to serum harvested from mice that had been given a PGPE-enriched diet elicited reduced osteoclast differentiation and bone resorption, as shown by the inhibition of the major osteoclast markers. In addition, PGPE appeared to substantially stimulate osteoblastic MC3T3-E1 alkaline phosphatase (ALP) activity at day 7, mineralization at day 21 and the transcription level of osteogenic markers. PGPE may be effective in preventing the bone loss associated with ovariectomy in mice, and offers a promising alternative for the nutritional management of this disease.
Highlights
Bone is a dynamic organ that is continuously and precisely remodelled by the combined roles of osteoblasts and osteoclasts
Incubation with serum from pomegranate peel extract (PGPE) animals did not modify the proliferation of the MC3T3-E1 cells, on days 2 and 7, in comparison with cells cultured with serum from CT mice (Figure 2A)
Using an ex vivo investigation that makes it possible to address the overall physiological conditions coupled with a well-described preclinical model, we demonstrated that dietary PGPE could improve bone mass and microarchitecture with transcriptional changes in bone tissue during osteoporosis establishment
Summary
Bone is a dynamic organ that is continuously and precisely remodelled by the combined roles of osteoblasts and osteoclasts. Imbalance in bone remodelling is usually caused by a deregulated coupling between the main bone cells due to an increase in osteoclast resorption activity over the bone-formation rate by osteoblasts or by low bone turnover where both formation and resorption are reduced. This process leads to a common adult bone disease, i.e., osteoporosis [1], which is a systemic skeletal disorder characterized by low bone mass and the structural deterioration of the microarchitecture, leading to bone fragility [2]. It has been shown that polyphenolic compounds such as flavonoids, more precisely, genistein, daidzein, oleuropein, hydroxytyrosol, and others, exert an effect on osteoporosis [4,5,6,7,8,9], inhibit osteoclast differentiation [10,11,12] and stimulate osteoblast formation [13,14,15,16] in vitro and in vivo
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