Activation of NLRP1 and NLRP3 inflammasomes contributed to cyclic stretch-induced pyroptosis and release of IL-1β in human periodontal ligament cells

Zhao, Dan; Wu, Yaqin; Zhuang, Jiabao; Xu, Chun; Zhang, Fuqiang

doi:10.18632/oncotarget.11944

Cited by 44 publications

(35 citation statements)

References 34 publications

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“…Inflammasomes have been reported to be involved in both inflammation and programmed cell death [ 26 , 27 , 28 ]. Because intracellular ROS generation has been explored as one of the factors for NLRP3 inflammasome activation, we first examined, using Western blot analysis, whether purpurin treatment will lead to down-regulation of the inflammasome assembly scaffold and activation in RAW 264.7 cells [ 29 ].…”

Section: Resultsmentioning

confidence: 99%

Structure-Antioxidative and Anti-Inflammatory Activity Relationships of Purpurin and Related Anthraquinones in Chemical and Cell Assays

et al. 2017

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Anthraquinone (9,10-anthraquinone) and several hydroxy derivatives, including purpurin (1,2,4-trihydroxyanthraquinone), anthrarufin (1,5-dihydroxyanthraquinone), and chrysazin (1,8-dihydroxyanthraquinone), were evaluated for antioxidative and anti-inflammatory activities in chemical assays and mammalian cells (murine macrophage RAW 264.7 cells). Several tests were used to assess their activities: 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical; ABTS radical cation; hydrogen peroxide scavenging; reduction of potassium ferricyanide; chelation of ferrous ions; inhibition of lipid peroxidation; inhibition of nitric oxide generation; scavenging of the intracellular hydroxyl radical; expression of NLRP3 polypeptide for inflammasome assembly; and quantitation of proinflammatory cytokine interleukin 1β (IL-1β) for inflammasome activation. The results show that purpurin, from the root of the madder plant (Rubia tinctorum L.), exhibited the highest antioxidative activity in both chemical and cultured cell antioxidant assays. The antioxidative activities of the other three anthraquinones were lower than that of purpurin. In addition, purpurin could down-regulate NLRP3 inflammasome assembly and activation, suggesting that it might protect foods against oxidative damage and prevent in vivo oxidative stress and inflammation. Structure-activity relationships and the significance of the results for food quality and human health are discussed.

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Section: Resultsmentioning

confidence: 99%

Structure-Antioxidative and Anti-Inflammatory Activity Relationships of Purpurin and Related Anthraquinones in Chemical and Cell Assays

et al. 2017

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“…Glyburide suppresses NLRP3‐dependent caspase‐1 activation and IL‐1β expression in mouse bone marrow‐derived macrophages after stimulation with LPS and ATP . Activation of NLRP3 inflammasomes following mechanical stimulation has been observed in cultured human PDL cells . Although we found numerous IL‐1β‐positive cells in the PDL of the T group on day 5, there were significantly fewer positive cells in the T + G group.…”

Section: Discussionmentioning

confidence: 57%

Glyburide inhibits the bone resorption induced by traumatic occlusion in rats

Arita

Yoshinaga

Kaneko

et al. 2020

J of Periodontal Research

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Objective To examine whether glyburide inhibits bone destruction caused by traumatic occlusion in a rat occlusal trauma model. Background Excessive mechanical stress, such as traumatic occlusion, induces expression of IL‐1β and may be involved in bone resorption. NLRP3 inflammasomes have been linked to IL‐1β expression, but it is currently unclear whether glyburide, the inhibiter of NLRP3 inflammasome, suppresses occlusal trauma in rats. Methods Male SD rats aged 7 weeks were used. In the trauma group, the occlusal surface of the maxillary first right molar was raised by attaching a metal wire to apply occlusal trauma to the mandibular first right molar. In the trauma + glyburide group, the NLRP3 inhibitor glyburide was administered orally every 24 hours from 1 day before induction of occlusal trauma. Rats were euthanized after 5 or 10 days, and the maxillary first molars were harvested with the adjacent tissues for histopathological investigation. Immunohistochemical expression of IL‐1β, NLRP3, and RANKL was also assessed. Results On day 5, bone resorption was significantly greater in the trauma group compared with the control group or the trauma + glyburide group, and there were significantly higher numbers of osteoclasts and cells positive for IL‐1β, NLRP3, and RANKL in the trauma group. Conclusion In this study, glyburide inhibits bone resorption by traumatic occlusion in rats. It suggests that the NLRP3/IL‐1β pathway might be associated with bone resorption induced by traumatic occlusion.

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“…Despite a high morphological similarity, a caspase-1-dependent and a caspase-1-independent pyroptosis have particular features as following described. One of the most important steps is to bind caspase-1 nucleotides to the oligomeric receptor (NLR) family during pyrophosphate-dependent activation, absent in melanoma 2 (AIM2) or pyrin, NLRP1 and NLRP3 inflammatory bodies were activated by human periodontal ligament cells and subjected to cyclic stretch [9,10]. NLRC4 responds to bacterial flagellin or components of bacterial type III secretion systems [11].…”

Section: Morphological and Molecular Features Of Pyroptosismentioning

confidence: 99%

Roles of pyroptosis in myocardial ischemia/reperfusion injury diseases

Shi

Zhang

Gao

et al. 2019

Preprint

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Ischemia-reperfusion injury (IRI) occurred when an organ lost its blood supply in a short time, and then the perfusion was restored automatically or iatrogenically, leading to a burst of reactive oxygen species (ROS) from mitochondria. It is common in the clinic, and lead to deterioration, even death, so an exploratory examination of the mechanism of ischemia-reperfusion injury is of great significance. Among the most common and fatal types of IR in myocardial tissue, myocardial IRI is one of the most fatal diseases in the modern world. The cellular and molecular mechanisms of IRI mainly include calcium overload, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, energy metabolic disorders, neutrophil infiltration, cardiomyocyte autophagy, and apoptosis, etc. The main pathogenesis of IRI is programmed cell death, of which apoptosis is the most deeply studied processes. However, pyroptosis is a highly inflammatory form of programmed cell death (PCD), which depends on the activation of the caspase cascade and inflammatory mediators, which have been thought to be involved in the processes of IRI. Ptosis has been referred to as a pattern. PCD with apoptosis characteristics Necrosis. It’s stimulated by molecular signaling pathways similar to apoptosis, mainly including Caspase. The research progress in recent years is presented in this review. Among them, myocardial tissue and so on provide a theoretical basis for the burning organ system in I/R injury and provide theoretical practice for the clinical research of reducing ischemia-reperfusion injury.

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Activation of NLRP1 and NLRP3 inflammasomes contributed to cyclic stretch-induced pyroptosis and release of IL-1β in human periodontal ligament cells

Cited by 44 publications

References 34 publications

Structure-Antioxidative and Anti-Inflammatory Activity Relationships of Purpurin and Related Anthraquinones in Chemical and Cell Assays

Structure-Antioxidative and Anti-Inflammatory Activity Relationships of Purpurin and Related Anthraquinones in Chemical and Cell Assays

Glyburide inhibits the bone resorption induced by traumatic occlusion in rats

Roles of pyroptosis in myocardial ischemia/reperfusion injury diseases

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