Protection against osteoporosis by statins is linked to a reduction of oxidative stress and restoration of nitric oxide formation in aged and ovariectomized rats

Yin, Hong; Shi, Zhen‐Guo; Yu, Yongsheng; Hu, Jing; Wang, Ru; Luan, Zhi-Peng; Guo, Dai-Hong

doi:10.1016/j.ejphar.2011.11.024

Cited by 53 publications

(28 citation statements)

References 41 publications

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“…[25] and MG-63 cells [26]. In addition, in their studies, treatment with simvastatin significantly prevented the apoptotic effects of H 2 O 2 in the cells [25,26]. In the present study, we demonstrated the protective effect of simvastatin against Hcy-induced increases in Nox1 and Nox2 expressions and apoptosis of osteocytic cells, suggesting that simvastatin has anti-apoptotic effects on not only osteoblasts but also osteocytes by reducing oxidative stress.…”

Section: Discussionsupporting

confidence: 55%

“…In addition, we showed for the first time that simvastatin ameliorated the Hcy-induced apoptosis and the upregulation of Nox1 and Nox2 in MLO-Y4 cells. [25] and MG-63 cells [26]. In addition, in their studies, treatment with simvastatin significantly prevented the apoptotic effects of H 2 O 2 in the cells [25,26].…”

Section: Discussionmentioning

confidence: 98%

“…Statistical evaluations for differences between groups were performed using one-way ANOVA foland/or activity in various cell types [21][22][23][24], including osteoblasts [25,26]. Therefore, we hypothesized that statins might prevent Hcy-induced apoptosis.…”

Section: Statisticsmentioning

confidence: 99%

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Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

et al. 2016

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 98%

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Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

et al. 2016

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“…It has been demonstrated that chemicals promoting ROS, such as rotenone and H 2 O 2 , decrease cell viability, reduce mitochondrial membrane potential, and further cause osteoblast apoptosis (Dawson et al, 1993). The association of oxidative stress was also reconfirmed by the oxidative stress inhibition by protective agents against osteoporosis (Yin et al, 2012;Chavan et al, 2007). Therefore, the anti-oxidative stress agents might promise to prevent and control osteoporosis.…”

Section: Introductionmentioning

confidence: 85%

Grape seed proanthocyanidins inhibit H2O2-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H2O2-induced mitochondrial dysfunction

et al. 2014

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-Oxidative stress represents a major cause of cellular damage and death in pathological conditions including osteoporosis, in which oxidative stress is associated with increased bone resorption and low bone mass. And grape seed proanthocyanidins are a group of polyphenolic bioflavonoids which are known to possess broad pharmacological activity and therapeutic potential, exerting a protective role against oxidant injury. The aim of our study was to investigate whether proanthocyanidins exert an anti-apoptosis effect in osteoblastic MC3T3-E1 cells, via their antioxidant activity. Firstly, we determined the anti-apoptosis effect of proanthocyanidins in osteoblastic MC3T3-E1 cells, which were subject to H 2 O 2 treatment, then we determined the association of the antioxidant activity exerted by proanthocyanidins with their anti-apoptosis effect. Results demonstrated that proanthocyanidins inhibit H 2 O 2 -promoted apoptosis in MC3T3-E1 cells, via ameliorating the viability of MC3T3-E1 cells post H 2 O 2 treatment and reducing the apoptotic cell numbers. And the proanthocyanidins treatment also ameliorates the H 2 O 2 -induced mitochondrial dysfunction via promoting the mitochondrial membrane potential (MMP) and respiratory chain complex IV, and reducing the mitochondrial free radical production, ROS and mitochondrial superoxide. Moreover, the proanthocyanidins inhibit H 2 O 2 -induced apoptosis signaling which is mediated by p53. This study implied a possible anti-osteoporosis effect of proanthocyanidins via their antioxidant and anti-apoptosis activity.

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“…Furthermore, a multitude of studies have reported that the increased production of reactive oxygen species (ROS) and, proinflammatory cytokine, as well as the activation of MAPKs may lead to bone loss and osteoporosis in vitro or in vivo [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

17β-estradiol attenuates homocysteine-induced oxidative stress and inflammatory response as well as MAPKs cascade via activating PI3-K/Akt signal transduction pathway in Raw 264.7 cells

Zhang¹,

He²,

Zong³

et al. 2015

ABBS

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Oxidative stress, inflammatory response, and mitogen-activated protein kinases (MAPKs) cascade are significant pathogenic factors of osteoporosis. It has been reported that elevated homocysteine (Hcy) may activate oxidative stress and reduce bone mineral density in post-menopausal osteoporosis. Moreover, hormone replacement therapy has been widely used in clinic to prevent and treat post-menopausal women with osteoporosis and osteoporotic fracture, but the molecular mechanisms and relevant signal transduction pathways underlying the action of Hcy remain unclear. In this study, we investigated the effects of 17β-estradiol (17β-E 2 ) on the Hcy-induced oxidative stress, inflammatory response and MAPKs cascade, as well as the underlying signal transduction pathway in murine Raw 264.7 cells. The reactive oxygen species (ROS) was assessed by fluorospectrophotometry. The proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β were analyzed by double-immunofluorescence labeling and reverse transcriptase polymerase chain reaction assay, respectively. Furthermore, phosphorylation levels of MAPKs cascade were measured by western blot analysis. A specific phosphatidylinositol 3-kinase (PI3-K) inhibitor, Wortmannin (1 μM) was employed to determine whether PI3-K/Akt signaling pathway mediated the 17β-E 2 's effect on Raw 264.7 cells. 17β-E 2 markedly decreased the ROS production induced by Hcy, the expression of TNF-α and IL-1β at protein and mRNA levels, and down-regulated the phosphorylation of MAPKs (ERK1/2, JNK and p38). These suppressing effects of 17β-E 2 on Hcy-induced changes were reversed by pretreatment with PI3-K inhibitor Wortmannin. The results indicate that 17β-estradiol may attenuate Hcy-induced oxidative stress, inflammatory response and up-regulation of MAPKs in Raw 264.7 cells via PI3-K/Akt signal transduction pathway.

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Protection against osteoporosis by statins is linked to a reduction of oxidative stress and restoration of nitric oxide formation in aged and ovariectomized rats

Cited by 53 publications

References 41 publications

Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

Grape seed proanthocyanidins inhibit H<sub>2</sub>O<sub>2</sub>-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H<sub>2</sub>O<sub>2</sub>-induced mitochondrial dysfunction

17β-estradiol attenuates homocysteine-induced oxidative stress and inflammatory response as well as MAPKs cascade via activating PI3-K/Akt signal transduction pathway in Raw 264.7 cells

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Protection against osteoporosis by statins is linked to a reduction of oxidative stress and restoration of nitric oxide formation in aged and ovariectomized rats

Cited by 53 publications

References 41 publications

Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

Simvastatin rescues homocysteine-induced apoptosis of osteocytic MLO-Y4 cells by decreasing the expressions of NADPH oxidase 1 and 2

Grape seed proanthocyanidins inhibit H<sub>2</sub>O<sub>2</sub>-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H<sub>2</sub>O<sub>2</sub>-induced mitochondrial dysfunction

17&beta;-estradiol attenuates homocysteine-induced oxidative stress and inflammatory response as well as MAPKs cascade via activating PI3-K/Akt signal transduction pathway in Raw 264.7 cells

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17β-estradiol attenuates homocysteine-induced oxidative stress and inflammatory response as well as MAPKs cascade via activating PI3-K/Akt signal transduction pathway in Raw 264.7 cells