ROS-induced NLRP3 inflammasome priming and activation mediate PCB 118- induced pyroptosis in endothelial cells

Long, Yang; Liu, Xin; Tan, Xiaozhen; Jiang, Chunxia; Chen, Shaowei; Liang, Guannan; He, Xuemei; Wu, Jian; Chen, Tao; Xu, Yong

doi:10.1016/j.ecoenv.2019.109937

Cited by 83 publications

(50 citation statements)

References 34 publications

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“…They seem to accompany one another and promote each other in many chronic diseases Biswas, 2016;Steven et al, 2019;Zuo et al, 2019). ROS may serve as a "kindling" to activate NLRP3 inflammasomes, leading to pro-inflammatory cytokine secretion (IL-1β and IL-18) (Abais et al, 2015;Long et al, 2020). ROS may also induce the activation of nuclear factor kappa B (NF-κB), a crucial mediator of inflammatory responses, and is associated with the pathogenesis of many disorders (Liu T et al, 2017;Liang et al, 2017;Qin et al, 2017).…”

Section: Oxidative Stress and Inflammation In The Ovariesmentioning

confidence: 99%

The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging

et al. 2021

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The ovarian system comprises vital organs in females and is of great significance for the maintenance of reproductive potential and endocrine stability. Although complex pathogenesis undoubtedly contributes to ovarian aging, increasing attention is being paid to the extensive influence of oxidative stress. However, the role of oxidative stress in ovarian aging is yet to be fully elucidated. Exploring oxidative stress-related processes might be a promising strategy against ovarian aging. In this review, compelling evidence is shown that oxidative stress plays a role in the etiology of ovarian aging and promotes the development of other ovarian aging-related etiologies, including telomere shortening, mitochondrial dysfunction, apoptosis, and inflammation. In addition, some natural antioxidants such as quercetin, resveratrol, and curcumin have a protective role in the ovaries through multiple mechanisms. These findings raise the prospect of oxidative stress modulator-natural antioxidants as therapeutic interventions for delaying ovarian aging.

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Section: Oxidative Stress and Inflammation In The Ovariesmentioning

confidence: 99%

The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging

et al. 2021

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“…In the context of ARDS, the weight of evidence suggests that excessive PIC and ROS damage to cellular proteins and DNA also results in massively increased intracellular mtROS production and the subsequent activation of the NLPR 3 inflammasome [ 244 , 245 ]. This is an important point as inflammasome activation and the release of IL-1 and IL-18 appear to make a significant contribution to the development and progression of ARDS in the later stages of disease and high levels of the latter cytokine is associated with an extremely poor prognosis [ [246] , [247] , [248] ].…”

Section: The Recruitment Of Activated Neutrophils Into Alveolae and Imentioning

confidence: 99%

“…There would appear to be many elements underpinning the association between increased inflammasome activity and mortality in ARDS patients. Perhaps the most important is spirally increasing cell death by pyroptosis and necrosis, most notably in macrophages and epithelial cells [ 244 , 245 ].…”

Section: The Recruitment Of Activated Neutrophils Into Alveolae and Imentioning

confidence: 99%

The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach

Morris

Bortolasci

Puri³

et al. 2020

Life Sciences

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In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed.

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“…It has been proved that caspase-1 activity in dependent inflammasome can lead to cell death in a highly inflammatory form called pyroptosis. 25 In the process of pyroptosis, cleave caspase-1 could trigger the maturation and secretion of IL-1β and IL-18 and then expand inflammatory reaction. 26 And the inhibition of caspase-1 could slow down the development of chronic arthritis.…”

Section: F I G U R Ementioning

confidence: 99%

Activating Nrf2 signalling alleviates osteoarthritis development by inhibiting inflammasome activation

Yan

Zhan

et al. 2020

J Cellular Molecular Medi

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Osteoarthritis (OA), which is characterized by proliferation of subchondral bone and the degeneration of articular cartilage, is the most prevalent human arthritis. Nod‐like receptor pyrin domain 3 (NLRP3) inflammasome is a hot spot in recent year and has been reported to be associated with OA synovial inflammation. However, there are few studies on NLRP3 inflammasome in chondrocyte. Licochalcone A (Lico A), a compound extracted from Glycyrrhiza species, has various biological effects such as anti‐inflammation, anti‐apoptotic, anti‐cancer and anti‐oxidation. In this study, we investigated the protective effect of Lico A on chondrocytes stimulated by lipopolysaccharide (LPS) and surgically induced OA models. In vitro, Lico A could reduce the expression of NLRP3, apoptosis‐associated speck‐like protein (ASC), Gasdermin D (GSDMD), caspase‐1, interleukin‐1beta (IL‐1β) and IL‐18, which indicated that Lico A attenuates LPS‐induced chondrocytes pyroptosis. In addition, Lico A ameliorates the degradation of extracellular matrix (ECM) by enhancing the expression of aggrecan and collagen‐II. Meanwhile, we found that Lico A inhibits NLRP3 inflammasome via nuclear factor erythroid‐2‐related factor 2 (Nrf2)/haeme oxygenase‐1(HO‐1)/nuclear factor kappa‐B (NF‐κB) axis. And the Nrf2 small interfering RNA (siRNA) could reverse the anti‐pyroptosis effects of Lico A in mouse OA chondrocytes. In vivo, Lico A mitigates progression OA in a mouse model and reduces OA Research Society International (OARSI) scores. Thus, Lico A may have therapeutic potential in OA.

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ROS-induced NLRP3 inflammasome priming and activation mediate PCB 118- induced pyroptosis in endothelial cells

Cited by 83 publications

References 34 publications

The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging

The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging

The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach

Activating Nrf2 signalling alleviates osteoarthritis development by inhibiting inflammasome activation

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