Correlation between bone mineral density and oxidative stress in postmenopausal women

Sharma, Tripti; Islam, Najmul; Ahmad, Jamal; Akhtar, Nishat; Beg, M. Salim

doi:10.4103/2230-8210.159053

Cited by 33 publications

(14 citation statements)

References 21 publications

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“…Studies have found that it is significantly elevated in the serum of women with OP after menopause (Ozgocmen et al 2007; Sendur et al 2009). The antioxidant enzymes SOD and GPX scavenge free radicals, and their levels have been found to be significantly lower in the serum of women with OP after menopause than in healthy postmenopausal women (Sharma et al 2015). If excessive free radical production exceeds the coping ability of the natural antioxidant defense mechanism, bone resorption may occur (Sheweita and Khoshhal 2007).…”

Section: Discussionmentioning

confidence: 99%

Melatonin prevents bone destruction in mice with retinoic acid–induced osteoporosis

Wang

Liang

Zhu

et al. 2019

Mol Med

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Background The protective effect of melatonin against bone metabolism imbalance in osteoporosis (OP) induced by drugs such as retinoic acid (RA) is unclear. The aim of this study was to explore the role of melatonin in bone destruction based on a mouse model. Methods RA-induced OP model mice were established. To assess the effect of melatonin on these mice, micro-CT was used to characterize the trabecular structure of normal mice and those treated with RA (model), RA + low-dose melatonin (Mlt-L), RA + high-dose melatonin (Mlt-H), and RA + alendronate sodium (positive control). The shape of the trabecular bone, the length and diameter of the femoral head and the height and diameter of vertebra(L1) of each group were also measured and the number of osteoclasts was determined by Tartrate-resistant acid phosphatase (TRACP) staining. Meanwhile, the expression of alkaline phosphatase (ALP) was evaluated by immunohistochemistry assays. The differences between groups in terms of liver and kidney oxidation–related indexes and serum and urinary indicators related to bone metabolism were also analyzed. Furthermore, qRT-PCR and western blotting were used to evaluate the effect of melatonin on osteogenic and osteoclastic differentiation in MC3T3-E1 and RAW264.7 cells, respectively. Results RA induction led to a decrease in the amount and density of trabecular bone, a decrease in the length and diameter of the femur and height, diameter of the vertebra (L1), a decrease in bone mass and density and the expression of ALP, and an increase in the number of osteoclasts. Melatonin treatment alleviated these effects induced by RA, increasing the amount of trabecular bone in OP mice, improving the microstructure of the femur and vertebra(L1) and increasing bone mass bone density and the expression of ALP, as well as decreasing the number of osteoclasts. Additionally, blood and urinary bone metabolism-related indicators showed that melatonin promoted bone formation and inhibited bone resorption. Determination of oxidant and antioxidant biomarkers in the livers and kidneys of the mice revealed that melatonin promoted the antioxidant level and suppressed the level of oxidant molecules in these organs. In vitro, RA promoted osteoclasts and inhibit osteogenesis by increasing oxidative stress levels in the RAW264.7 and MC3T3-E1 cells, but melatonin reversed this effect. Melatonin may, therefore, play a role in the ERK/SMAD and NF-κB pathways. Conclusions Melatonin can alleviate bone loss in RA-induced OP model mice, repair the trabecular microstructure, and promote bone formation. These effects may be related to reducing oxidation levels in vivo and vitro through the ERK/SMAD and NF-κB pathways. Electronic supplementary material The online version of this article (10.1186/s10020-019-0107-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Melatonin prevents bone destruction in mice with retinoic acid–induced osteoporosis

Wang

Liang

Zhu

et al. 2019

Mol Med

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“…Epidemiological and genetic studies of humans and rodents have indicated that ROS accumulation and increased oxidative stress play critical roles in the development of osteoporosis (Lee et al., 2015; Sharma et al., 2015). In bone tissues, excessive ROS production directly promotes osteoblast and bone-cell apoptosis (Sato et al., 2015).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Ameliorates Glucocorticoid-Induced Bone Damage in a Zebrafish Model

et al. 2019

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Resveratrol (Res) is a multi-functional polyphenol compound that has protective functions in cardiovascular and neurodegenerative diseases. This study aimed to determine the effect of Res on osteogenic differentiation and bone mineralization in zebrafish ( Danio rerio ) with dexamethasone (Dex)-induced bone damage. Our results showed that Dex exposure (15 μmol/l) decreased the green fluorescence areas and the integrated optic density (IOD) values in the skull bones of zebrafish larvae of the TG(SP7:EGFP) strain in a dose-dependent manner ( p < 0.01). Furthermore, Dex exposure decreased the alizarin red S-stained areas (bone mineralization area) in the skeleton and spinal bones of zebrafish larvae of the AB strain in a dose-dependent manner ( p < 0.01). By contrast, Res treatment (150 μmol/l) significantly increased both the green fluorescence and bone mineralization area in Dex-exposed zebrafish larvae. Thus, our data show that Res improves bone mineralization after glucocorticoid-induced bone damage in a zebrafish model. Res may be a candidate drug for the prevention of osteoporosis.

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“…The effect of both dietary fat and CoQ 10 might be related to reactive oxygen species (ROS) roles on bone resorption. Several pieces of evidence link oxidative stress to BMD decrease in humans [ 43 , 44 ]. In addition, its association with age-dependent decline of bone mass and strength in sex steroid-sufficient female or male mice has been also reported [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Loss of Bone Mineral Density Associated with Age in Male Rats Fed on Sunflower Oil Is Avoided by Virgin Olive Oil Intake or Coenzyme Q Supplementation

Varela-López

Ochoa

Elvira

et al. 2017

IJMS

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The role of dietary fat unsaturation and the supplementation of coenzyme Q have been evaluated in relation to bone health. Male Wistar rats were maintained for 6 or 24 months on two diets varying in the fat source, namely virgin olive oil, rich in monounsaturated fatty acids, or sunflower oil, rich in n-6 polyunsaturated fatty acids. Both dietary fats were supplemented or not with coenzyme Q10 (CoQ10). Bone mineral density (BMD) was evaluated in the femur. Serum levels of osteocalcin, osteopontin, receptor activator of nuclear factor κB ligand (RANKL), osteoprotegerin (OPG), adrenocorticotropin (ACTH) and parathyroid hormone (PTH), as well as urinary F2-isoprostanes were measured. Aged animals fed on virgin olive oil showed higher BMD than those fed on sunflower oil. In addition, CoQ10 prevented the age-related decline in BMD in animals fed on sunflower oil. Urinary F2-isoprostanes analysis showed that sunflower oil led to the highest oxidative status in old animals, which was avoided by supplementation with CoQ10. In conclusion, lifelong feeding on virgin olive oil or the supplementation of sunflower oil on CoQ10 prevented, at least in part mediated by a low oxidative stress status, the age-related decrease in BMD found in sunflower oil fed animals.

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Correlation between bone mineral density and oxidative stress in postmenopausal women

Cited by 33 publications

References 21 publications

Melatonin prevents bone destruction in mice with retinoic acid–induced osteoporosis

Melatonin prevents bone destruction in mice with retinoic acid–induced osteoporosis

Resveratrol Ameliorates Glucocorticoid-Induced Bone Damage in a Zebrafish Model

Loss of Bone Mineral Density Associated with Age in Male Rats Fed on Sunflower Oil Is Avoided by Virgin Olive Oil Intake or Coenzyme Q Supplementation

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