Phospholipid peroxidation-driven modification of chondrogenic transcription factor mediates alkoxyl radicals-induced impairment of embryonic bone development

Niu, Jie; Wan, Xin; Yu, Guiyuan; Jiang, Shan; Yi, Ruo-Nan; Wu, Yanping; Ouyang, Shu-Hua; Liu, Liang; Kojima, Hiroshi; Sun, Wanyang; Zhu, Xiaofeng; Cao, Yun‐Feng; He, Jianbo; Duan, Wen-Jun; Li, Yi-Fang; He, Rong‐Rong

doi:10.1016/j.redox.2022.102437

Cited by 7 publications

(3 citation statements)

References 67 publications

(70 reference statements)

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“…We found that RJP significantly inhibited lipid ROS induced by AAPH and t-BuOOH, as well as the levels of lipid peroxidation metabolites MDA and 4-HNE. Several studies have demonstrated that AAPH, t-BuOOH, and 4-HNE can induce oxidative cell death [46][47][48]. Through ORAC experiments, RJP was found to enhance the clearance ability of lipid radicals of lysates of HDFs stressed by H 2 O 2 and t-BuOOH.…”

Section: Discussionmentioning

confidence: 93%

Antioxidant and Anti-Inflammatory Properties of Hydrolyzed Royal Jelly Peptide in Human Dermal Fibroblasts: Implications for Skin Health and Care Applications

Yan,

Zhu,

Guan

et al. 2024

Bioengineering

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Hydrolyzed royal jelly peptide (RJP) has garnered attention for its health-promoting functions. However, the potential applications of RJP in skincare have not been fully explored. In this study, we prepared RJP through the enzymatic hydrolysis of royal jelly protein with trypsin and investigated its antioxidant and anti-inflammatory properties on primary human dermal fibroblasts (HDFs). Our results demonstrate that RJP effectively inhibits oxidative damage induced by H2O2 and lipid peroxidation triggered by AAPH and t-BuOOH in HDFs. This effect may be attributed to the ability of RJP to enhance the level of glutathione and the activities of catalase and glutathione peroxidase 4, as well as its excellent iron chelating capacity. Furthermore, RJP modulates the NLRP3 inflammasome-mediated inflammatory response in HDFs, suppressing the mRNA expressions of NLRP3 and IL-1β in the primer stage induced by LPS and the release of mature IL-1β induced by ATP, monosodium urate, or nigericin in the activation stage. RJP also represses the expressions of COX2 and iNOS induced by LPS. Finally, we reveal that RJP exhibits superior antioxidant and anti-inflammatory properties over unhydrolyzed royal jelly protein. These findings suggest that RJP exerts protective effects on skin cells through antioxidative and anti-inflammatory mechanisms, indicating its promise for potential therapeutic avenues for managing oxidative stress and inflammation-related skin disorders.

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Section: Discussionmentioning

confidence: 93%

Antioxidant and Anti-Inflammatory Properties of Hydrolyzed Royal Jelly Peptide in Human Dermal Fibroblasts: Implications for Skin Health and Care Applications

Yan,

Zhu,

Guan

et al. 2024

Bioengineering

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“…In a recent study, Geib et al [ 89 ] identified 4-HNE-modified proteins such as 4-HNE-modified histones, H2A and H2B, and histone deacetylase in chondrocytes of OA patients via anti-4-HNE antibodies. Moreover, Niu et al [ 90 ] recently found that 4-HNE has a role in dampening chondrogenesis. Their results demonstrated that 4-HNE could form adducts with SOX9 and lead to its ubiquitin-mediated degradation [ 90 ].…”

Section: Pathological Aspects Of Lipid Peroxidation In Oamentioning

confidence: 99%

“…Moreover, Niu et al [ 90 ] recently found that 4-HNE has a role in dampening chondrogenesis. Their results demonstrated that 4-HNE could form adducts with SOX9 and lead to its ubiquitin-mediated degradation [ 90 ].…”

Section: Pathological Aspects Of Lipid Peroxidation In Oamentioning

confidence: 99%

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

Zhang,

Hou,

Guo

et al. 2023

Cell Death Discov.

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Osteoarthritis (OA) is a multifactorial and increasingly prevalent degenerative disease that affects the whole joint. The pathogenesis of OA is poorly understood and there is a lack of therapeutic interventions to reverse the pathological process of this disease. Accumulating studies have shown that the overproduction of reactive oxygen species (ROS) and ROS-induced lipid peroxidation are involved in the pathogenesis of OA. 4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) have received considerable attention for their role in cartilage degeneration and subchondral bone remodeling during OA development. Ferroptosis is a form of cell death characterized by a lack of control of membrane lipid peroxidation and recent studies have suggested that chondrocyte ferroptosis contributes to OA progression. In this review, we aim to discuss lipid peroxidation-derived 4-HNE and MDA in the progression of OA. In addition, the therapeutic potential for OA by controlling the accumulation of lipid peroxidation and inhibiting chondrocyte ferroptosis are discussed.

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Supplementation with carnosine, a food‐derived bioactive dipeptide, alleviates dexamethasone‐induced oxidative stress and bone impairment via the NRF2 signaling pathway

Li,

Gu,

et al. 2024

J Sci Food Agric

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BACKGROUNDCarnosine, a natural bioactive dipeptide derived from meat muscle, possesses strong antioxidant properties. Dexamethasone, widely employed for treating various inflammatory diseases, raises concerns regarding its detrimental effects on bone health. This study aimed to investigate the protective effects of carnosine against dexamethasone‐induced oxidative stress and bone impairment, along with its underlying mechanisms, utilizing chick embryos and a zebrafish model in vivo, as well as MC3T3‐E1 cells in vitro.RESULTSOur findings revealed that carnosine effectively mitigated bone injury in dexamethasone‐exposed chick embryos, accompanied by reduced oxidative stress. Further investigation demonstrated that carnosine alleviated impaired osteoblastic differentiation in MC3T3‐E1 cells and zebrafish by suppressing the excessive production of reactive oxygen species (ROS) and enhancing the activity of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPX). Moreover, mechanistic studies elucidated that carnosine promoted the expression and nuclear translocation of nuclear factor erythroid 2‐related factor 2 (NRF2), thereby facilitating the transcription of its downstream antioxidant response elements, including heme oxyense‐1 (HO‐1), glutamate cysteine ligase modifier (GCLM), and glutamate cysteine ligase catalytic (GCLC) to counteract dexamethasone‐induced oxidative stress.CONCLUSIONOverall, this study underscores the potential therapeutic efficacy of carnosine in mitigating oxidative stress and bone damage induced by dexamethasone exposure, shedding light on its underlying mechanism of action by activating the NRF2 signaling pathway. © 2024 Society of Chemical Industry.

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Phospholipid peroxidation-driven modification of chondrogenic transcription factor mediates alkoxyl radicals-induced impairment of embryonic bone development

Cited by 7 publications

References 67 publications

Antioxidant and Anti-Inflammatory Properties of Hydrolyzed Royal Jelly Peptide in Human Dermal Fibroblasts: Implications for Skin Health and Care Applications

Antioxidant and Anti-Inflammatory Properties of Hydrolyzed Royal Jelly Peptide in Human Dermal Fibroblasts: Implications for Skin Health and Care Applications

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis

Supplementation with carnosine, a food‐derived bioactive dipeptide, alleviates dexamethasone‐induced oxidative stress and bone impairment via the NRF2 signaling pathway

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