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Bone. 2016 Feb;83:127-140. doi: 10.1016/j.bone.2015.10.017. Epub 2015 Nov 5.

Lycopene treatment against loss of bone mass, microarchitecture and strength in relation to regulatory mechanisms in a postmenopausal osteoporosis model.

Author information

1
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Clinical Biochemistry, King Abdulaziz University, Jeddah, Saudi Arabia; King Abdulaziz University Hospital, King Abdulaziz University, Jeddah, Saudi Arabia. Electronic address: msmardawi@yahoo.com.
2
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Anatomy, King Abdulaziz University, Jeddah, Saudi Arabia.
3
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Obstetrics and Gynecology, King Abdulaziz University, Jeddah, Saudi Arabia; King Abdulaziz University Hospital, King Abdulaziz University, Jeddah, Saudi Arabia.
4
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia.
5
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Haematology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; King Abdulaziz University Hospital, King Abdulaziz University, Jeddah, Saudi Arabia.
6
Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia; Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, State of New York University, Rensselaer, NY, USA.

Abstract

Lycopene supplementation decreases oxidative stress and exhibits beneficial effects on bone health, but the mechanisms through which it alters bone metabolism in vivo remain unclear. The present study aims to evaluate the effects of lycopene treatment on postmenopausal osteoporosis. Six-month-old female Wistar rats (n=264) were sham-operated (SHAM) or ovariectomized (OVX). The SHAM group received oral vehicle only and the OVX rats were randomized into five groups receiving oral daily lycopene treatment (mg/kg body weight per day): 0 OVX (control), 15 OVX, 30 OVX, and 45 OVX, and one group receiving alendronate (ALN) (2μg/kg body weight per day), for 12weeks. Bone densitometry measurements, bone turnover markers, biomechanical testing, and histomorphometric analysis were conducted. Micro computed tomography was also used to evaluate changes in microarchitecture. Lycopene treatment suppressed the OVX-induced increase in bone turnover, as indicated by changes in biomarkers of bone metabolism: serum osteocalcin (s-OC), serum N-terminal propeptide of type 1 collagen (s-PINP), serum crosslinked carboxyterminal telopeptides (s-CTX-1), and urinary deoxypyridinoline (u-DPD). Significant improvement in OVX-induced loss of bone mass, bone strength, and microarchitectural deterioration was observed in lycopene-treated OVX animals. These effects were observed mainly at sites rich in trabecular bone, with less effect in cortical bone. Lycopene treatment down-regulated osteoclast differentiation concurrent with up-regulating osteoblast together with glutathione peroxidase (GPx) catalase (CAT) and superoxide dismutase (SOD) activities. These findings demonstrate that lycopene treatment in OVX rats primarily suppressed bone turnover to restore bone strength and microarchitecture.

KEYWORDS:

Bone mass and microarchitecture; Bone turnover; Lycopene; Osteoclastogenesis; Ovariectomy; Oxidative stress

PMID:
26549245
DOI:
10.1016/j.bone.2015.10.017
[Indexed for MEDLINE]

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