Dihydromyricetin inhibits NLRP3 inflammasome‐dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells

Hu, Qin; Zhang, Ting; Lv, Yi; Zhou, Xi; Mi, Mantian

doi:10.1002/biof.1395

Cited by 146 publications

(94 citation statements)

References 60 publications

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“…The results from other present studies indicate that DHM improves pyroptosis and concomitantly alleviates IL-1β secretion by activating the Nrf2 signaling pathway to inhibit ROS-dependent NLRP3 inflammasome activation in palmitic acid (PA) induced HUVECs [23]. LncRNA revealed in several recent studies can function as a molecular sponge or a competing endogenous RNA (ceRNA) in modulating expression and biological functions of miRNAs [24].…”

Section: Morphological and Molecular Features Of Pyroptosismentioning

confidence: 59%

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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Section: Morphological and Molecular Features Of Pyroptosismentioning

confidence: 59%

Roles of pyroptosis in myocardial ischemia/reperfusion injury diseases

Shi

Zhang

Gao

et al. 2019

Preprint

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“…DHM inhibited PA-induced high-temperature cell death by increasing cell viability and reducing caspase-1 and IL-1β release to improve cell membrane integrity. is study showed that DHM pretreatment significantly reduced intracellular ROS and mtROS levels and activated the Nrf2 signaling pathway [104]. In summary, these results suggested that the Nrf2 signaling pathway was obviously partially involved in the DHM-mediated improvement of PA-induced vascular events, suggesting the potential medicinal value of DHM against immune/inflammation-related diseases such as atherosclerosis.…”

Section: Natural Medicine and The Treatment For Asmentioning

confidence: 64%

NLRP3 Inflammasome: A Potential Alternative Therapy Target for Atherosclerosis

Yang

Yin

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Atherosclerosis (AS) is a complex and chronic inflammatory disease that occurs in multiple systems of the human body. It is an important pathological basis for a variety of diseases and a serious threat to human health. So far, many theories have been formed to explain the pathogenesis of atherosclerosis, among which “inflammation theory” has gradually become a research focus. This theory presents that inflammatory response runs through the whole progress of AS, inflammatory cells play as the main executors of AS, and inflammatory mediators are the key molecules of AS. In the inflammatory process of atherosclerosis, the role of NLRP3 in the atherosclerosis has gradually got the attention of researchers. NLRP3 is a kind of signal-transductional pattern recognition receptors (PRRs). After recognizing and binding to the damage factors, NLRP3 inflammasome will be assembled to activate IL-1β and caspase-1 pathways, resulting in promoting the inflammation process of AS, reducing the stability of the plaques, and finally increasing the incidence of adverse cardiovascular events. Taken above, the article will review the potential benefits of drugs targeting the NLRP3 inflammasome in the therapy of AS.

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“…Beside, studies also showed the regulation effect of Nrf2 on pyroptosis. It was shown activating the Nrf2 signaling pathway could inhibit NLRP3 inflammasome‐dependent pyroptosis in vascular endothelial cells . Li et al also demonstrated erythropoietin could rescue primary rat cortical neurons by regulation of pyroptosis through Erk1/2‐Nrf2/Bach1 signal pathway .…”

Section: Discussionmentioning

confidence: 99%

“…It was shown activating the Nrf2 signaling pathway could inhibit NLRP3 inflammasome-dependent pyroptosis in vascular endothelial cells. 48 Li et al also demonstrated erythropoietin could rescue primary rat cortical neurons by regulation of pyroptosis through Erk1/2-Nrf2/ Bach1 signal pathway. 13 In our study, we for the first time showed At last, we also demonstrated the effects of CPF on miR-181 and revealed the regulation effects of miR-181 on SIRT1/PGC-1α/Nrf2 pathway, cell pyroptosis, and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Chlorpyrifos activates cell pyroptosis and increases susceptibility on oxidative stress‐induced toxicity by miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in human neuroblastoma SH‐SY5Y cells

Zhao

Yang

Zhao

2019

Environmental Toxicology

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Background The insecticide exposure has been linked to Parkinson's disease (PD). In the present study, we used a most widely used cell line in study of PD, the SH‐SY5Y cells, to investigate mechanisms of chlorpyrifos (CPF) induced cell toxicity and the possible roles of cell pyroptosis and oxidative stress in SH‐SY5Y cells, as well as role of miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in this process. Methods SH‐SY5Y cells were treated with different concentrations of CPF. Cell viability was measured using CCK‐8 assay. Cell pyroptosis was determined by immunofluorescence of caspase‐1 and TUNEL assay. The miR‐181 (has‐miR‐181‐5p) level was determined by qRT‐PCR. Expression of SIRT1, PGC‐1α, Nrf2, and pyroptosis related proteins NLRP3, caspase‐1, IL‐1β, and IL‐18 was determined by both qRT‐PCR and Western blotting. Results Cell viability was found to be decreased with the increased CPF concentrations. The pyroptosis related proteins, ROS levels, as well as level of caspase‐1 and the TUNEL positive cells were all significantly up‐regulated by CPF. Meanwhile, expression of miR‐181 and pyroptosis proteins was also enhanced, while the SIRT1/PGC‐1α/Nrf2 signaling was inhibited by CPF. Knockdown of Nrf2 significantly up‐regulated the expression of pyroptosis related proteins, ROS level, caspase‐1, and the TUNEL positive cells, while over‐expression of Nrf2 resulted in opposite results. The expression of PGC‐1α and Nrf2 was significantly down‐regulated when SIRT1 was inhibited, while over‐expressed SIRT1 led to increased PGC‐1α and Nrf2 levels. Besides, miR‐181 promoted the CPF induced activation of pyroptosis and oxidative stress, as well as down‐regulated SIRT1/PGC‐1α/Nrf2 signaling, while inhibition of miR‐181 led to opposite results. Conclusions Chlorpyrifos could inhibit cell proliferation, activate cell pyroptosis and increase susceptibility on oxidative stress‐induced toxicity by elevating miR‐181 through down‐regulation of the SIRT1/PGC‐1α/Nrf2 pathway in human neuroblastoma SH‐SY5Y cells. This study might give deeper insights for mechanisms of CPF induced toxicity and might give some novel research targets for PD treatment.

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Dihydromyricetin inhibits NLRP3 inflammasome‐dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells

Cited by 146 publications

References 60 publications

Roles of pyroptosis in myocardial ischemia/reperfusion injury diseases

Roles of pyroptosis in myocardial ischemia/reperfusion injury diseases

NLRP3 Inflammasome: A Potential Alternative Therapy Target for Atherosclerosis

Chlorpyrifos activates cell pyroptosis and increases susceptibility on oxidative stress‐induced toxicity by miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in human neuroblastoma SH‐SY5Y cells

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