Diallyl trisulfide inhibits monosodium urate-induced NLRP3 inflammasome activation via NOX3/4-dependent mitochondrial oxidative stress in RAW 264.7 and bone marrow-derived macrophages

Kim, Min Yeong; Bang, EunJin; Hwangbo, Hyun; Ji, Seon Yeong; Kim, Da Hye; Lee, Hyesook; Park, Cheol; Hong, Su Hyun; Kim, Gi‐Young; Choi, Yung Hyun

doi:10.1016/j.phymed.2023.154705

Cited by 7 publications

(5 citation statements)

References 35 publications

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“…The first description of Nox3 expression in an immune cell type was made by van Buul et al, which detected Nox3 in the T-cell cancer line Jurkat [508]. Miyano and colleagues firstly showed that Nox3 is expressed and active in innate immune cells, namely the macrophagelike cancer cell line RAW 246.7 [275], which was confirmed in later studies [520,521]. In contrast, Nox3 mRNA was not detected in ex vivo Kupffer macrophages [460], and since no other ex vivo cell analysis was performed until now, it remains unclear if Nox3 belongs to the basic Nox repertoire of macrophages or if it is more part of the cancerous phenotype of RAW cells.…”

Section: Nox3 In Immune Cellsmentioning

confidence: 89%

“…Ye and colleagues investigated the interplay between oxidative and anti-oxidative responses in rat kidney after phenol-induced kidney injury [492] and detected an increase of Nox2, Nox3, p22 phox and p47 phox mRNA in isolated brain nuclei. Kim et al detected a protein up-regulation of Nox3 after mono sodium urate crystal treatment in RAW cells [520]. Some bioactive, substances isolated from medical plants, such as Brevilin A [548] or Genipin [521], also induced Nox3 mRNA and/or protein up-regulation.…”

Section: Up-regulation Nox3 On the Expression Levelmentioning

confidence: 99%

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NADPH Oxidase 3: Beyond the Inner Ear

Herb

2024

Antioxidants

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Reactive oxygen species (ROS) were formerly known as mere byproducts of metabolism with damaging effects on cellular structures. The discovery and description of NADPH oxidases (Nox) as a whole enzyme family that only produce this harmful group of molecules was surprising. After intensive research, seven Nox isoforms were discovered, described and extensively studied. Among them, the NADPH oxidase 3 is the perhaps most underrated Nox isoform, since it was firstly discovered in the inner ear. This stigma of Nox3 as “being only expressed in the inner ear” was also used by me several times. Therefore, the question arose whether this sentence is still valid or even usable. To this end, this review solely focuses on Nox3 and summarizes its discovery, the structural components, the activating and regulating factors, the expression in cells, tissues and organs, as well as the beneficial and detrimental effects of Nox3-mediated ROS production on body functions. Furthermore, the involvement of Nox3-derived ROS in diseases progression and, accordingly, as a potential target for disease treatment, will be discussed.

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Section: Nox3 In Immune Cellsmentioning

confidence: 89%

Section: Up-regulation Nox3 On the Expression Levelmentioning

confidence: 99%

NADPH Oxidase 3: Beyond the Inner Ear

Herb

2024

Antioxidants

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“…ROS production in the total of the cells and mitochondria was detected using DCF-DA (Thermo Fisher Scientific, Waltham, MA, USA) and MitoSox (Molecular Probes, Eugene, OR, USA) fluorescence probes, respectively. The experimental procedures followed the previous study [ 39 ].…”

Section: Methodsmentioning

confidence: 99%

Spermidine Attenuates High Glucose-Induced Oxidative Damage in Retinal Pigment Epithelial Cells by Inhibiting Production of ROS and NF-κB/NLRP3 Inflammasome Pathway

Bang

Park

Hwangbo

et al. 2023

IJMS

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Diabetic retinopathy (DR) is the leading cause of vision loss and a critical complication of diabetes with a very complex etiology. The build-up of reactive oxygen species (ROS) due to hyperglycemia is recognized as a primary risk factor for DR. Although spermidine, a naturally occurring polyamine, has been reported to have antioxidant effects, its effectiveness in DR has not yet been examined. Therefore, in this study, we investigated whether spermidine could inhibit high glucose (HG)-promoted oxidative stress in human retinal pigment epithelial (RPE) cells. The results demonstrated that spermidine notably attenuated cytotoxicity and apoptosis in HG-treated RPE ARPE-19 cells, which was related to the inhibition of mitochondrial ROS production. Under HG conditions, interleukin (IL)-1β and IL-18’s release levels were markedly increased, coupled with nuclear factor kappa B (NF-κB) signaling activation. However, spermidine counteracted the HG-induced effects. Moreover, the expression of nucleotide-binding oligomerization domain-like receptor (NLR) protein 3 (NLRP3) inflammasome multiprotein complex molecules, including TXNIP, NLRP3, ASC, and caspase-1, increased in hyperglycemic ARPE-19 cells, but spermidine reversed these molecular changes. Collectively, our findings demonstrate that spermidine can protect RPE cells from HG-caused injury by reducing ROS and NF-κB/NLRP3 inflammasome pathway activation, indicating that spermidine could be a potential therapeutic compound for DR treatment.

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“…Similarly, mitochondrial ROS production was measured using the MitoSox red dye (Thermo Fisher Scientific, Waltham, MA, USA), which detects the level of superoxide anions in the mitochondria. At the end of treatment, the cells were stained with MitoSox (10 µM), and the fluorescence intensity was analyzed via flow cytometry and fluorescence microscopy [30].…”

Section: Ros Assaymentioning

confidence: 99%

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

et al. 2023

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Diabetic retinopathy (DR) is the leading cause of vision loss and a major complication of diabetes. Hyperglycemia-induced accumulation of reactive oxygen species (ROS) is an important risk factor for DR. β-asarone, a major component of volatile oil extracted from Acori graminei Rhizoma, exerts antioxidant effects; however, its efficacy in DR remains unknown. In this study, we investigated whether β-asarone inhibits high-glucose (HG)-induced oxidative damage in human retinal pigment epithelial (RPE) ARPE-19 cells. We found that β-asarone significantly alleviated cytotoxicity, apoptosis, and DNA damage in HG-treated ARPE-19 cells via scavenging of ROS generation. β-Asarone also significantly attenuated the excessive accumulation of lactate dehydrogenase and mitochondrial ROS by increasing the manganese superoxide dismutase and glutathione activities. HG conditions markedly increased the release of interleukin (IL)-1β and IL-18 and upregulated their protein expression and activation of the nuclear factor-kappa B (NF-κB) signaling pathway, whereas β-asarone reversed these effects. Moreover, expression levels of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome multiprotein complex molecules, including thioredoxin-interacting protein, NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, and cysteinyl aspartate-specific proteinase-1, were increased in ARPE-19 cells under HG conditions. However, their expression levels remained similar to those in the control group in the presence of β-asarone. Therefore, β-asarone protects RPE cells from HG-induced injury by blocking ROS generation and NF-κB/NLRP3 inflammasome activation, indicating its potential as a therapeutic agent for DR treatment.

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Diallyl trisulfide inhibits monosodium urate-induced NLRP3 inflammasome activation via NOX3/4-dependent mitochondrial oxidative stress in RAW 264.7 and bone marrow-derived macrophages

Cited by 7 publications

References 35 publications

NADPH Oxidase 3: Beyond the Inner Ear

NADPH Oxidase 3: Beyond the Inner Ear

Spermidine Attenuates High Glucose-Induced Oxidative Damage in Retinal Pigment Epithelial Cells by Inhibiting Production of ROS and NF-κB/NLRP3 Inflammasome Pathway

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

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