Protective Effect of Pyrroloquinoline Quinone on TNF-α-induced Mitochondrial Injury in Chondrocytes

Han, Guoge; Cai, Weisong; Zhang, Yu-Biao; Zhou, Siqi; He, Binglin; Li, Haohuan

doi:10.1007/s11596-020-2248-3

Cited by 9 publications

(5 citation statements)

References 31 publications

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“…TNF-α was also found to stimulate NF-κB mediated inflammatory response and ERS in human chondrocytes. [81] In another study Han communicated that in TNF-α-treated chondrocytes mitochondria cristae and ATP decreased as consequence of the mitochondria injury [82].…”

Section: Ultrastructural Damages In Chondrocytes Exposed To Os Were C...mentioning

confidence: 99%

Ultrasound Protects Human Chondrocytes from Biochemical and Ultrastructural Changes Induced by Oxidative Stress

et al. 2022

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The aim of the study was to assess the effects of therapeutic ultrasound (US) on oxidative stress (OS)-induced changes in cultured human chondrocytes (HCH). For this, monolayer HCH were randomized in three groups: a control group (CG), a group exposed to OS (OS group), and a group exposed to US and OS (US-OS group). US exposure of the chondrocytes was performed prior to OS induction by hydrogen peroxide. Transmission electron microscopy (TEM) was used to assess the chondrocytes ultrastructure. OS and inflammatory markers were recorded. Malondialdehyde (MDA) and tumor necrosis factor (TNF)-α were significantly higher (p < 0.05) in the OS group than in CG. In the US-OS group MDA and TNF-α were significantly lower (p < 0.05) than in the OS group. Finally, in the US-OS group MDA and TNF-α were lower than in CG, but without statistical significance. TEM showed normal chondrocytes in CG. In the OS group TEM showed necrotic chondrocytes and chondrocytes with a high degree of vacuolation and cell organelles damages. In the US-OS group the chondrocytes ultrastructure was well preserved, and autophagosomes were generated. In conclusion, US could protect chondrocytes from biochemical (lipid peroxidation, inflammatory markers synthesis) and ultrastructural changes induced by OS and could stimulate autophagosomes development.

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Section: Ultrastructural Damages In Chondrocytes Exposed To Os Were C...mentioning

confidence: 99%

Ultrasound Protects Human Chondrocytes from Biochemical and Ultrastructural Changes Induced by Oxidative Stress

et al. 2022

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“…Furthermore, promoting mitochondrial fusion and inhibiting fission has been shown to improve mitochondrial function and reduce cartilage matrix degradation [27]. Compounds capable of modulating mitochondrial metabolism and improving mitochondrial function, such as nicotinamide riboside and pyrroloquinoline quinone, have also been investigated in the context of OA [85,86]. These compounds promote mitochondrial biogenesis, enhance mitochondrial respiration, and reduce oxidative stress and inflammation in chondrocytes, ultimately preserving the integrity of the cartilage matrix.…”

Section: Mitochondrial Metabolism and Cartilage Matrix Degradation In...mentioning

confidence: 99%

The role and intervention of mitochondrial metabolism in osteoarthritis

Zhu

Cai

et al. 2023

Mol Cell Biochem

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Osteoarthritis (OA), a prevalent degenerative joint disease, affects a substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as a significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles in cellular metabolism. Hence, mitochondrial dysfunction can exert broad-ranging effects on various cellular processes implicated in OA development. This comprehensive review aims to provide an overview of the metabolic alterations occurring in OA and elucidate the diverse mechanisms through which mitochondrial dysfunction can contribute to OA pathogenesis. These mechanisms encompass heightened oxidative stress and inflammation, perturbed chondrocyte metabolism, and compromised autophagy. Furthermore, this review will explore potential interventions targeting mitochondrial metabolism as means to impede or decelerate the progression of OA. In summary, this review offers a comprehensive understanding of the involvement of mitochondrial metabolism in OA and underscores prospective intervention strategies.

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“…29 More recently, osteoarthritis, a degenerative disease of cartilage has shown that supplemental PQQ can relieve mitochondrion damage and increase the number of mitochondria, preserve ATP levels and reduce pro-inflammatory cytokines like tumor necrosis factor (TNF-α). 30 Related work on TNF-α has looked at how PQQ can delay inflammaging which is a low level pro-inflammatory state where inflammatory factors are released into tissues. Their work shows that PQQ can extend the lifespan of nematodes by reducing senescence and the expression and proliferation of TNF-α.…”

Section: Understanding Cirs and Mould Biotoxinsmentioning

confidence: 99%

Pyrroloquinoline Quinone (PQQ): a novel approach to managing chronic inflammatory response syndrome and mitochondrial dysfunction

Jones¹

2023

JBMOA

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Chronic Inflammatory Response Syndrome (CIRS) is a complex, multi-system condition associated with persistent inflammation in response to biotoxins like mould or other environmental triggers. Mitochondrial dysfunction has been implicated in the pathophysiology of CIRS, contributing to chronic inflammation and exacerbating symptoms. Pyrroloquinoline quinone (PQQ), a redox cofactor, has gained attention for its potential neuroprotective, anti-inflammatory, and mitochondria-supporting properties. Additionally, CIRS shares overlapping features with cytokine storm effects observed in COVID infection, long COVID, and potential inflammatory reactions related to mRNA vaccine administration. This letter explores the role of PQQ in managing CIRS and addressing mitochondrial dysfunction caused by multiple potential triggers. However, further research is needed to confirm the effectiveness and safety of PQQ in addressing CIRS and related conditions.

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Protective Effect of Pyrroloquinoline Quinone on TNF-α-induced Mitochondrial Injury in Chondrocytes

Cited by 9 publications

References 31 publications

Ultrasound Protects Human Chondrocytes from Biochemical and Ultrastructural Changes Induced by Oxidative Stress

Ultrasound Protects Human Chondrocytes from Biochemical and Ultrastructural Changes Induced by Oxidative Stress

The role and intervention of mitochondrial metabolism in osteoarthritis

Pyrroloquinoline Quinone (PQQ): a novel approach to managing chronic inflammatory response syndrome and mitochondrial dysfunction

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