Antioxidants, like coenzyme Q10, selenite, and curcumin, inhibited osteoclast differentiation by suppressing reactive oxygen species generation

Moon, Ho Jin; Ko, Wan Kyu; Han, Song Wook; Kim, Duck-Su; Hwang, Yu‐Shik; Park, Hun Kuk; Kwon, Il Keun

doi:10.1016/j.bbrc.2012.01.005

Cited by 97 publications

(69 citation statements)

References 20 publications

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“…Curcumin might decrease bone resorption by inhibition of osteoclast proliferation, differentiation, and activity as well as by promotion of osteoclast apoptosis [44][45][46][47]. Although no consistent conclusion has been reached concerning its benefits in osteogenesis, our present findings demonstrate that curcumin significantly decreases osteoblast apoptosis induced by H 2 O 2 with similar effectiveness as the antioxidant compound EUK134.…”

Section: Discussionsupporting

confidence: 58%

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Dai

Mao

Sun

et al. 2017

Cell Physiol Biochem

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Background: Osteoblast apoptosis induced by oxidative stress plays a crucial role in the development and progression of osteoporosis. Curcumin, a natural antioxidant isolated from Curcuma longa, has highly protective effects against osteoporosis. However, the effects of curcumin on oxidative stressinduced osteoblast apoptosis remain unclear. This study aimed to explore the effect of curcumin on hydrogen peroxide (H 2 O 2 ) induced osteoblast apoptosis and the underlying mechanisms. Methods: An osteoblastic cell line (Saos-2) was exposed to various concentrations of H 2 O 2 with or without curcumin treatment. Cell viability was evaluated by MTT assays. The apoptosis rate was analyzed by flow cytometry and TUNEL assays. Mitochondrial ROS and membrane potential were determined using a fluorescence microscope. Mitochondrial respiratory enzyme activity was measured using a spectrophotometer. Protein levels were detected by western blotting. Results: Curcumin was cytoprotective because it greatly improved the viability of Saos-2 cells exposed to H 2 O 2 and attenuated H 2 O 2 -induced apoptosis. Curcumin treatment also preserved the mitochondrial redox potential, decreased the mitochondrial oxidative status, and improved the mitochondrial membrane potential and functions. Furthermore, curcumin treatment markedly increased levels of phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3β (GSK3β). Conclusion: Curcumin administration ameliorates oxidative stress-induced apoptosis in osteoblasts by preserving mitochondrial functions and activation of Akt-GSK3β signaling. These data provide experimental evidence supporting the clinical use of curcumin for prevention or treatment of osteoporosis.P. Dai and Y. Mao contributed equally to this work.

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Section: Discussionsupporting

confidence: 58%

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Dai

Mao

Sun

et al. 2017

Cell Physiol Biochem

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“…Curcumin also acts as an inhibitor of RANKL-induced NFATc1 which is a downstream event of NF-κB signal pathway through suppressing of ROS generation [24], leading to suppressed proliferation, induced chemosensitization, and suppressed osteoclastogenesis [25][26][27]. Osteoclasts are activated by binding of the RANKL [28] to its cognate receptor, RANK, whereas OPG, a soluble member of the tumor necrosis receptor super-family, acts as a naturally occurring decoy receptor that competes with RANK for binding of RANKL [29].…”

Section: Discussionmentioning

confidence: 99%

Attenuation of hind-limb suspension-induced bone loss by curcumin is associated with reduced oxidative stress and increased vitamin D receptor expression

et al. 2015

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“…20 This effect attenuates ROS-induced NF-kB signaling pathways for osteoclastogenesis and then causes a decrease in NFATc1 gene expression, which is the master gene involved in the osteoclastic differentiation. Figure 1 Chemical structure of curcumin.…”

Section: Effects Of Curcumin On Bonementioning

confidence: 99%

Therapeutic actions of curcumin in bone disorders

2016

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Curcumin is the active component of turmeric extract derived from the Curcuma longa plant. In the last decade, curcumin has raised a considerable interest in medicine owing to its negligible toxicity and multiple therapeutic actions including anti-cancer, anti-inflammatory and anti-microbial activities. Among the various molecular targets of curcumin, some are involved in bone remodeling, which strongly suggests that curcumin can affect the skeletal system. The review sheds light on the current and potential applications of curcumin to treat bone disorders characterized by an excessive resorption activity. Within the scope of this review, the novel formulations of curcumin to overcome its physico-chemical and pharmacokinetic constraints are also discussed.

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Antioxidants, like coenzyme Q10, selenite, and curcumin, inhibited osteoclast differentiation by suppressing reactive oxygen species generation

Cited by 97 publications

References 20 publications

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Attenuation of hind-limb suspension-induced bone loss by curcumin is associated with reduced oxidative stress and increased vitamin D receptor expression

Therapeutic actions of curcumin in bone disorders

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