Resveratrol prevents RANKL-induced osteoclast differentiation of murine osteoclast progenitor RAW 264.7 cells through inhibition of ROS production

He, Xu; Andersson, Göran; Lindgren, Urban; Li, Yan

doi:10.1016/j.bbrc.2010.09.053

Cited by 135 publications

(79 citation statements)

References 33 publications

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“…This finding is similar to data presented by Singh who reported inhibition of the collagen type I, osteopontin, and bone sialoprotein formation by 2,3,7,8-tetrachlorodibenzo-p-dioxin from cigarette smoke, this effect was antagonized by resveratrol [27]. Moreover, resveratrol is also able to inhibit the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclast differentiation, induces osteoclast apoptosis by inhibition of ROS production [28], activates osteoblastic activity in vitro by bone transcription of core binding factor α-1 (Cbfa-1) [14], and reduce rosiglitazone-induced oxidative stress in osteoblast-like cells [29]. The resveratrol induces bone morphogenetic protein-2 through Src kinase-dependent estrogen receptor activation [30] and it could play a role in protecting against bone loss induced by estrogen deficiency [31], which arose after BDO.…”

Section: Discussionsupporting

confidence: 91%

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

Zivna

Mičuda²,

Brcakova-Dolezelova³

et al. 2013

OJEMD

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Objective: We studied the influence of bile duct obstruction (BDO) after 28 days on bone metabolism status and their modification by resveratrol in male Wistar rats. Methods: The rats were divided into 3 groups: Sham group with laparotomy and vehiculum application, group BDO-bile duct obstruction and vehiculum application, and group R-BDO-bile duct obstruction and resveratrol application (10 mg/kg dose of resveratrol orally once daily). The bone mineral density (BMD; g/cm 2 ) and body composition were measured by dual energy X-ray absorptiometry. The physiccal strenght of femur was examined by controlled break biomechanical testing. The osteocalcin, procollagen type I N-terminal propeptide (PINP) and carboxy-terminal collagen crosslinks (CTX) were analysed by EIA in the bone tissue homogenate.

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Section: Discussionsupporting

confidence: 91%

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

Zivna

Mičuda²,

Brcakova-Dolezelova³

et al. 2013

OJEMD

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“…54 Thus, following stimulation with RANKL, the pre-osteoclasts increase intracellular ROS by activation of NADPH oxidase (Nox) homologs or by increased mitochondria ROS production, which subsequently induced long lasting Ca 2+ oscillations. [54][55][56] In the present study both intracellular ROS and Ca 2+ content of osteoclast-like cells cultured on nano-HA disks and nano-SiHA disks were analyzed by Flow Cytometry and higher values of both parameters were obtained in cells cultured on nano-SiHA than on nano-HA ( Fig. 9B and 9C).…”

Section: Intracellular Ros and Camentioning

confidence: 61%

Nanocrystalline silicon substituted hydroxyapatite effects on osteoclast differentiation and resorptive activity

Matesanz¹,

Linares

Lilue³

et al. 2014

J. Mater. Chem. B

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In the present study, the effects of nanocrystalline hydroxyapatite (nano-HA) and nanocrystalline Si-substituted hydroxyapatite (nano-SiHA) on osteoclast differentiation and resorptive activity have been evaluated in vitro using osteoclast-like cells. The action of these materials on proinflammatory and reparative macrophage populations was also studied. NanoSiHA disks delayed the osteoclast differentiation and decreased the resorptive activity of these cells on their surface, as compared to nano-HA samples, without affecting cell viability. Powdered nano-SiHA also induced an increase of the reparative macrophage population. These results along with the beneficial effects on osteoblasts previously observed with powdered nano-SiHA suggest the potential of this biomaterial for modulating the fundamental processes of bone formation and turnover, preventing bone resorption and enhancing bone formation at implantation sites in treatment of osteoporotic bone and in bone repair and regeneration.

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“…This could be explained because evidence has shown that resveratrol was capable of inhibiting osteoclast activity. Previous reports demonstrated that resveratrol inhibited osteoclast differentiation and decreased bone loss [12,13]. The inhibitory effect of resveratrol on osteoclast differentiation explained the decreased ALP level in vivo in resveratrol treated rats compared with OVX rats.…”

Section: Discussionmentioning

confidence: 96%

Protective effects of resveratrol on postmenopausal osteoporosis: regulation of SIRT1-NF-κB signaling pathway

Feng¹,

Liu²,

Ma³

et al. 2014

ABBS

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Postmenopausal osteoporosis severely jeopardizes human health. Seeking for therapeutic drugs without side effects is of great necessity. Our study was designed to investigate whether resveratrol, an agonist of SIRT1, could have favorable effect on osteoporosis and to explore the underlying mechanisms. Rat osteoporosis model (ovariectomy group, OVX) was established by bilateral ovariectomy. respectively; P < 0.05). Serum markers alkaline phosphatase (ALP) and osteocalcin were moderately restored by resveratrol. Moreover, resveratrol improved bone structure in OVX rats, demonstrated by hematoxylin-eosin staining and micro-computed tomographic results. In vitro results revealed that resveratrol promoted osteoblast differentiation of bone marrow mesenchymal stromal cells, evidenced by the increase of ALP generation and mRNA expression of collagen 1 (P < 0.05; RES MD , RES HD vs. control group). SIRT1 gene silencing by siRNA transfection blocked these beneficial effects of resveratrol (P < 0.05; RES 1 SIRT1 KD vs. RES HD ).Western blot results showed that resveratrol activated SIRT1 and subsequently suppressed the activity of NF-kB with decreased expression level of p-IkBa and NF-kB p65 (P < 0.05). Our findings verified the effects of specific dosed resveratrol on postmenopausal osteoporosis through osteoblast differentiation via SIRT1-NF-kB signaling pathway. This study suggested the therapeutic potential of resveratrol against osteoporosis and stressed the importance of effective doses.

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Resveratrol prevents RANKL-induced osteoclast differentiation of murine osteoclast progenitor RAW 264.7 cells through inhibition of ROS production

Cited by 135 publications

References 33 publications

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

Nanocrystalline silicon substituted hydroxyapatite effects on osteoclast differentiation and resorptive activity

Protective effects of resveratrol on postmenopausal osteoporosis: regulation of SIRT1-NF-κB signaling pathway

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Resveratrol prevents RANKL-induced osteoclast differentiation of murine osteoclast progenitor RAW 264.7 cells through inhibition of ROS production

Cited by 135 publications

References 33 publications

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

The Effect of Resveratrol on Bone Status in Rats with Bile Duct Obstruction

Nanocrystalline silicon substituted hydroxyapatite effects on osteoclast differentiation and resorptive activity

Protective effects of resveratrol on postmenopausal osteoporosis: regulation of SIRT1-NF-&kappa;B signaling pathway

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Protective effects of resveratrol on postmenopausal osteoporosis: regulation of SIRT1-NF-κB signaling pathway