MnTBAP inhibits bone loss in ovariectomized rats by reducing mitochondrial oxidative stress in osteoblasts

Cao, Xiangchang; Luo, Dingcun; Teng, Li; Huang, Zunxian; Zou, Weitao; Wang, Lei; Lian, Kun; Lin, Dasheng

doi:10.1007/s00774-019-01038-4

Cited by 18 publications

(14 citation statements)

References 53 publications

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“…It is currently recognised that the sperm mitochondria make a significant contribution to the ROS generation and oxidative stress in human spermatozoa (Aitken, 2020; Koppers et al., 2008). Since MnTBAP is a synthetic mitochondrial superoxide dismutase 2 (SOD2) mimic, we could hypothesise that the mechanism of action of this antioxidant is related to limit the mitochondrial oxidative stress, as has been reported in other cell types (Cao et al., 2020; Liu et al., 2018; Nguyen et al., 2015). Also, the beneficial effects of MnTBAP are attributed to a powerful antioxidant action on the cytoplasm and mitochondrion of the cell, since, in addition to turning O 2 ‐ into H 2 O 2 , it catalyses the dissociation of H 2 O 2 in water, blocking the damage produced by ROS (Forouzanfar et al., 2013; Shojaeian et al., 2018).…”

Section: Discussionmentioning

confidence: 85%

Protective effect of the superoxide dismutase mimetic MnTBAP during sperm vitrification process

et al. 2020

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Sperm cryopreservation is widely used in assisted reproduction and male infertility therapy; however, it induces oxidative stress affecting sperm quality. This work evaluated the effect of the antioxidant MnTBAP during vitrification steps in human spermatozoa. First, the effect of MnTBAP on viability and ROS production was evaluated. Then, the spermatozoa were vitrified in straws with the vitrification, warming and post-warming incubation media separately supplemented with MnTBAP. An untreated control was included. The sperm viability, ROS production, total and How to cite this article: Uribe P, Cárcamo C, Navarro E, et al. Protective effect of the superoxide dismutase mimetic MnTBAP during sperm vitrification process. Andrologia.

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Section: Discussionmentioning

confidence: 85%

Protective effect of the superoxide dismutase mimetic MnTBAP during sperm vitrification process

et al. 2020

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“…Many data relate high levels of reactive oxygen species (ROS) to defective bone remodeling and mineralization processes regulated by osteoblast and osteoclast activity [20][21][22][23][24], and controlled by osteocytes, through secretion of factors that can modulate both bone formation and resorption [25][26][27]. It has also been demonstrated that high levels of ROS induce marked apoptosis in osteoblasts and osteocytes [27][28][29][30], and both oxidative stress and osteocyte apoptosis are linked to deficiency of estrogens, the aging process and chronic glucocorticoid treatment with consequent decrease in bone mineral density [15,31,32].…”

Section: Introductionmentioning

confidence: 99%

Effect of Oxidative Stress-Induced Apoptosis on Active FGF23 Levels in MLO-Y4 Cells: The Protective Role of 17-β-Estradiol

Domazetovic

Falsetti

Ciuffi

et al. 2022

IJMS

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The discovery that osteocytes secrete phosphaturic fibroblast growth factor 23 (FGF23) has defined bone as an endocrine organ. However, the autocrine and paracrine functions of FGF23 are still unknown. The present study focuses on the cellular and molecular mechanisms involved in the complex control of FGF23 production and local bone remodeling functions. FGF23 was assayed using ELISA kit in the presence or absence of 17β–estradiol in starved MLO-Y4 osteocytes. In these cells, a relationship between oxidative stress-induced apoptosis and up-regulation of active FGF23 levels due to MAP Kinases activation with involvement of the transcriptional factor (NF-kB) has been demonstrated. The active FGF23 increase can be due to up-regulation of its expression and post-transcriptional modifications. 17β–estradiol prevents the increase of FGF23 by inhibiting JNK and NF-kB activation, osteocyte apoptosis and by the down-regulation of osteoclastogenic factors, such as sclerostin. No alteration in the levels of dentin matrix protein 1, a FGF23 negative regulator, has been determined. The results of this study identify biological targets on which drugs and estrogen may act to control active FGF23 levels in oxidative stress-related bone and non-bone inflammatory diseases.

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“…Oxidative stress, as a factor that affects bone remodelling, accelerates osteoporosis progression and plays a crucial role in the functional and morphological changes in osteoclasts in osteoporosis [ 41 , 42 ]. ROS, particularly hydrogen peroxide, are important contributors to the formation and differentiation of osteoclasts [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Mn-containing bioceramics inhibit osteoclastogenesis and promote osteoporotic bone regeneration via scavenging ROS

Deng

Liang

et al. 2021

Bioactive Materials

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Osteoporosis is caused by an osteoclast activation mechanism. People suffering from osteoporosis are prone to bone defects. Increasing evidence indicates that scavenging reactive oxygen species (ROS) can inhibit receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis and suppress ovariectomy-induced osteoporosis. It is critical to develop biomaterials with antioxidant properties to modulate osteoclast activity for treating osteoporotic bone defects. Previous studies have shown that manganese (Mn) can improve bone regeneration, and Mn supplementation may treat osteoporosis. However, the effect of Mn on osteoclasts and the role of Mn in osteoporotic bone defects remain unclear. In present research, a model bioceramic, Mn-contained β-tricalcium phosphate (Mn-TCP) was prepared by introducing Mn into β-TCP. The introduction of Mn into β-TCP significantly improved the scavenging of oxygen radicals and nitrogen radicals, demonstrating that Mn-TCP bioceramics might have antioxidant properties. The in vitro and in vivo findings revealed that Mn 2+ ions released from Mn-TCP bioceramics could distinctly inhibit the formation and function of osteoclasts, promote the differentiation of osteoblasts, and accelerate bone regeneration under osteoporotic conditions in vivo . Mechanistically, Mn-TCP bioceramics inhibited osteoclastogenesis and promoted the regeneration of osteoporotic bone defects by scavenging ROS via Nrf2 activation. These results suggest that Mn-containing bioceramics with osteoconductivity, ROS scavenging and bone resorption inhibition abilities may be an ideal biomaterial for the treatment of osteoporotic bone defect.

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MnTBAP inhibits bone loss in ovariectomized rats by reducing mitochondrial oxidative stress in osteoblasts

Cited by 18 publications

References 53 publications

Protective effect of the superoxide dismutase mimetic MnTBAP during sperm vitrification process

Protective effect of the superoxide dismutase mimetic MnTBAP during sperm vitrification process

Effect of Oxidative Stress-Induced Apoptosis on Active FGF23 Levels in MLO-Y4 Cells: The Protective Role of 17-β-Estradiol

Mn-containing bioceramics inhibit osteoclastogenesis and promote osteoporotic bone regeneration via scavenging ROS

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