Antioxidant α-lipoic acid inhibits osteoclast differentiation by reducing nuclear factor-κB DNA binding and prevents in vivo bone resorption induced by receptor activator of nuclear factor-κB ligand and tumor necrosis factor-α

Kim, Hyon J.; Chang, Eun‐Ju; Kim, Hyun‐Man; Lee, Seungbok; Kim, Hyun-Duck; Kim, Ghi Su; Kim, Hong-Hee

doi:10.1016/j.freeradbiomed.2005.10.066

Cited by 125 publications

(90 citation statements)

References 42 publications

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“…Since lipoic acid can boost glutathione levels via phase 2 induction, it is not surprising that lipoic acid has shown a favorable impact on maintenance of bone density in ovariectomized rats; this agent also opposes osteoclastogenesis in vitro (Kim et al 2006;Polat et al 2013). In 50 osteopenic postmenopausal women, randomized to receive an antioxidant regimen including lipoic acid + calcium/vitamin D or calcium/vitamin D alone, bone mass was significantly higher after 1 year in the patients receiving the antioxidants (Mainini et al 2012).…”

Section: Supplemental Nac In Aging Humans and Rodents Provides Versatmentioning

confidence: 99%

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

McCarty

DiNicolantonio

2015

AGE

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Restricted dietary intakes of protein or essential amino acids tend to slow aging and boost lifespan in rodents, presumably because they downregulate IGF-I/ Akt/mTORC1 signaling that acts as a pacesetter for aging and promotes cancer induction. A recent analysis of the National Health and Nutrition Examination Survey (NHANES) III cohort has revealed that relatively low protein intakes in mid-life (under 10 % of calories) are indeed associated with decreased subsequent risk for mortality. However, in those over 65 at baseline, such low protein intakes were associated with increased risk for mortality. This finding accords well with other epidemiology correlating relatively high protein intakes with lower risk for loss of lean mass and bone density in the elderly.

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Section: Supplemental Nac In Aging Humans and Rodents Provides Versatmentioning

confidence: 99%

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

McCarty

DiNicolantonio

2015

AGE

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Section: Resultsmentioning

confidence: 99%

“…Several studies have indicated that LA inhibits osteoclast differentiation in both in vitro and in vivo systems (Kim et al, 2006;Koh et al, 2005). Kim et al (2006) have demonstrated that this particular mechanism of osteoclastogenesis inhibition involves the suppression of NF-κB DNA binding. We speculate that LA suppresses NFATc1 expression in RANKL-induced osteoclastogenesis by downregulating NF-κB DNA binding, since NF-κB inhibitors regulate NFATc1 expression and inhibit bone resorption (Takatsuna et al, 2005).…”

Section: Resultsmentioning

confidence: 99%

“…Effective control of these excessive risk factors would have therapeutic value in overcoming various pathological etiologies of various erosive bone diseases (Rodan and Martin, 2000). Several recent reports indicate various functional foods and their active components that may be effective in such osteopathic treatments (Dong et al, 2008;Kim et al, 2003;Kim et al, 2006;Koh et al, 2005;Mühlbauer et al, 1999;Park et al, 2008;Tsuji-Naito, 2008;Yu et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…Their findings prompted investigation into the functionality of LA. Kim et al (2006) reported that LA suppresses osteoclastogenesis by suppressing NF-κB DNA binding, followed by the quenching of excessive reactive oxygen species production during mature osteoclast formation.…”

Section: Introductionmentioning

confidence: 99%

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Additive Inhibitory Effects of .ALPHA.-lipoic Acid with Cinnamaldehyde against Osteoclastogenesis

Naito

2010

FSTR

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This study characterized the intensive suppressive effects of α-lipoic acid (LA) and cinnamaldehyde (CA) on excessive osteoclastogenesis, specifically in the suppression of the nuclear factor of activated T cell 1 (NFATc1) expression, which acts a master transcriptional regulator of osteoclastogenesis. We confirmed that LA inhibited NFATc1 expression in the receptor activator of nuclear factor-κB ligand-stimulated RAW264.7 cells at concentrations of 50-100 μmol/L and that LA inhibited mature osteoclast formation. To enhance the effects of LA, we assessed the effects of LA when combined with CA. We found that a formulation containing 50 μmol/L LA and 5 μmol/L CA significantly suppressed both NFATc1 expression and mature osteoclast formation, in contrast to significant inhibition with 100 μmol/L LA or 10 μmol/L CA alone. Our results suggest that concomitant use of LA with CA may have therapeutic application for multiple bone disorders.

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3D Cryo‐Printed Hierarchical Porous Scaffolds Harmonized with Hybrid Nanozymes for Combinatorial Mitochondrial Therapy: Enhanced Diabetic Bone Regeneration via Micromilieu Remodeling

Deng,

Li,

Liu

et al. 2024

Adv Funct Materials

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Regeneration of bone defects in diabetic patients has always been a significant challenge in clinical treatment. The pathologic diabetic micromilieu, characterized by mitochondrial dysfunction, excessive reactive oxygen species (ROS) accumulation, cellular senescence, and chronic inflammation, compromises innate bone healing capacity. 3D cryo‐printing technology is utilized in bone tissue engineering to fabricate hierarchical porous scaffolds that promote a conducive microenvironment for cellular adhesion, migration, proliferation, and nutrient exchange. Nanozymes are used as synthetic mimics of natural enzymes to scavenge ROS, addressing the limitations of natural antioxidative enzymes. To remodel the diabetic bone regeneration micromilieu, a 3D cryo‐printed polyaryletherketone with carboxyl groups (PAEK‐COOH) and 45S5 bioactive glass (BG) hierarchical porous scaffold (PBG scaffold), harmonized with hybrid nanozymes comprising SS31‐enhanced manganese dioxide (MnO2)‐ferritin biomimetic nanozyme (MF@S nanozyme), is developed for combinatorial mitochondrial therapy. The MF@S nanozyme specifically targets mitochondria to enhance mitochondrial function, scavenge ROS accumulated in mitochondria, and suppress mitochondrial ROS (mtROS) production, and thus rejuvenate aging cells, regulate macrophage polarization, and modulate differentiation of osteoblasts and osteoclasts. This 3D cryo‐printed PBG‐MF@S hierarchical porous scaffold combines with a combinatorial mitochondrial therapy system to remodel the diabetic micromilieu and presents a promising therapeutic approach for the regeneration of bone defects in diabetes.

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Antioxidant α-lipoic acid inhibits osteoclast differentiation by reducing nuclear factor-κB DNA binding and prevents in vivo bone resorption induced by receptor activator of nuclear factor-κB ligand and tumor necrosis factor-α

Cited by 125 publications

References 42 publications

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

Additive Inhibitory Effects of .ALPHA.-lipoic Acid with Cinnamaldehyde against Osteoclastogenesis

3D Cryo‐Printed Hierarchical Porous Scaffolds Harmonized with Hybrid Nanozymes for Combinatorial Mitochondrial Therapy: Enhanced Diabetic Bone Regeneration via Micromilieu Remodeling

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