Cyanidin-3-glucoside Alleviates 4-Hydroxyhexenal-Induced NLRP3 Inflammasome Activation via JNK-c-Jun/AP-1 Pathway in Human Retinal Pigment Epithelial Cells

Jin, Xi; Wang, Chengtao; Wu, Wei; Liu, Tingting; Ji, Baoping; Zhou, Feng

doi:10.1155/2018/5604610

Cited by 34 publications

(19 citation statements)

References 44 publications

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“…There have been a few reports on the relationship between Ral and AP-1, 29 and between NLRP3 and AP-1. 30,31 However, no reports on the association among Ral, NLRP3, and AP-1 in CAC have been reported. Given our in vitro and in vivo results, the Ral-NLRP3 inflammasome interaction provides new insight into the elucidation of the CAC mechanism.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of RalGTPase-Activating Protein Promotes Colitis-Associated Cancer via NLRP3 Inflammasome Activation

Iida

Hirayama

Minami

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

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Ral activation impacts interleukin 1b production by nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome activation and enhances matrix metalloproteinase-9 and matrix metalloproteinase-13 expression in a newly established mouse colitis-associated cancer model. This study strongly showed that the Ras-likenucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome pathway is involved in the mechanism of colitis-associated cancer invasion. BACKGROUND & AIMS: Ral guanosine triphosphatase-activating protein a2 (RalGAPa2) is the major catalytic subunit of the negative regulators of the small guanosine triphosphatase Ral, a member of the Ras subfamily. Ral regulates tumorigenesis and invasion/ metastasis of some cancers; however, the role of Ral in colitisassociated cancer (CAC) has not been investigated. We aimed to elucidate the role of Ral in the mechanism of CAC. METHODS: We used wild-type (WT) mice and RalGAPa2 knockout (KO) mice that showed Ral activation, and bone marrow chimeric mice were generated as follows: WT to WT, WT to RalGAPa2 KO, RalGAPa2 KO to WT, and RalGAPa2 KO to RalGAPa2 KO mice. CAC was induced in these mice by intraperitoneal injection of azoxymethane followed by dextran sulfate sodium intake. Intestinal epithelial cells were isolated from colon tissues, and we performed complementary DNA microarray analysis. Cytokine expression in normal colon tissues and CAC was analyzed by quantitative polymerase chain reaction. RESULTS: Bone marrow chimeric mice showed that immune cell function between WT mice and RalGAPa2 KO mice was not significantly different in the CAC mechanism. RalGAPa2 KO mice had a significantly larger tumor number and size and a significantly higher proportion of tumors invading the submucosa than WT mice. Higher expression levels of matrix metalloproteinase-9 and matrix metalloproteinase-13 were observed in RalGAPa2 KO mice than in WT mice. The expression levels of interleukin 1b, NLRP3, apoptosis associated speck-like protein containing a CARD, and caspase-1 were apparently increased in the tumors of RalGAPa2 KO mice compared with WT mice. NLRP3 inhibitor reduced the number of invasive tumors. CONCLUSIONS: Ral activation participates in the mechanism of CAC development via NLRP3 inflammasome activation. (Cell

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Section: Discussionmentioning

confidence: 99%

Down-regulation of RalGTPase-Activating Protein Promotes Colitis-Associated Cancer via NLRP3 Inflammasome Activation

Iida

Hirayama

Minami

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

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“…Meanwhile, NLRP3 knockdown in A2E-treated ARPE-19 cells showed reduced ASC complex formation and IL-1β production [152]. Successful inhibition of NLRP3 was shown via inhibition of MAPK [146] and NF-κB [137] signaling pathways, as well as via treatments with cyanidin-3-glucoside [139] and puerarin-an antioxidant and anti-inflammatory compound [144].…”

Section: Nod-like Receptors In the Ocular Tissuesmentioning

confidence: 99%

“…Multiple pathways, including inflammation and oxidative stress, have been reported in AMD pathogenesis. In vitro, stimulation of RPE cells with LPS + TCDD (oxidative stress and low-grade inflammation), TNFα (inflammatory stress) [117], IL-1α (prime inflammasome components) [129,149], IL-17A (signature cytokine of Th17 cells) [136], 4-hydroxyhexenal (unsaturated aldehydes) [139], sodium iodate (NaIO 3 ; oxidative stress) [142], oxidized-low density lipoprotein (ox-LDL; modified lipoprotein) [138,145], C5a (complement factor) [140], Aβ 1-40 [144,146], all resulted in elevated NLRP3 expression. Meanwhile, NLRP3 knockdown in A2E-treated ARPE-19 cells showed reduced ASC complex formation and IL-1β production [152].…”

Section: Nod-like Receptors In the Ocular Tissuesmentioning

confidence: 99%

NOD-like Receptors in the Eye: Uncovering Its Role in Diabetic Retinopathy

Lim

Wieser

Ganga

et al. 2020

IJMS

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Diabetic retinopathy (DR) is an ocular complication of diabetes mellitus (DM). International Diabetic Federations (IDF) estimates up to 629 million people with DM by the year 2045 worldwide. Nearly 50% of DM patients will show evidence of diabetic-related eye problems. Therapeutic interventions for DR are limited and mostly involve surgical intervention at the late-stages of the disease. The lack of early-stage diagnostic tools and therapies, especially in DR, demands a better understanding of the biological processes involved in the etiology of disease progression. The recent surge in literature associated with NOD-like receptors (NLRs) has gained massive attraction due to their involvement in mediating the innate immune response and perpetuating inflammatory pathways, a central phenomenon found in the pathogenesis of ocular diseases including DR. The NLR family of receptors are expressed in different eye tissues during pathological conditions suggesting their potential roles in dry eye, ocular infection, retinal ischemia, cataract, glaucoma, age-related macular degeneration (AMD), diabetic macular edema (DME) and DR. Our group is interested in studying the critical early components involved in the immune cell infiltration and inflammatory pathways involved in the progression of DR. Recently, we reported that NLRP3 inflammasome might play a pivotal role in the pathogenesis of DR. This comprehensive review summarizes the findings of NLRs expression in the ocular tissues with special emphasis on its presence in the retinal microglia and DR pathogenesis.

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“…Cyanidin-3-glucoside has been found to inhibit NLRP3 inflammasome activation by reducing NLRP3, caspase-1, IL-1β, and IL-18 levels in 4-HNE-exposed ARPE-19 cells. This inhibitory mechanism may be mediated by regulating JNK-c-Jun/activator protein 1 (AP-1) pathway, further demonstrating the potential of cyanidin-3-glucoside to prevent retinal degenerative diseases [63,64]. Quercetin improves cell membrane integrity and mitochondrial function and decreases IL-6, IL-8, and monocyte chemotactic protein 1 (MCP-1) production, presumably by regulating MAPK/NF-κB signaling pathway in ARPE-19 cells stimulated by inflammatory cytokine [65].…”

Section: Prevention Of Eye Damagementioning

confidence: 99%

Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

Wang

et al. 2020

Biomolecules

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The toxic reactive aldehyde 4-hydroxynonenal (4-HNE) belongs to the advanced lipid peroxidation end products. Accumulation of 4-HNE and formation of 4-HNE adducts induced by redox imbalance participate in several cytotoxic processes, which contribute to the pathogenesis and progression of oxidative stress-related human disorders. Medicinal plants and bioactive natural compounds are suggested to be attractive sources of potential agents to mitigate oxidative stress, but little is known about the therapeutic potentials especially on combating 4-HNE-induced deleterious effects. Of note, some investigations clarify the attenuation of medicinal plants and bioactive compounds on 4-HNE-induced disturbances, but strong evidence is needed that these plants and compounds serve as potent agents in the prevention and treatment of disorders driven by 4-HNE. Therefore, this review highlights the pharmacological basis of these medicinal plants and bioactive compounds to combat 4-HNE-induced deleterious effects in oxidative stress-related disorders, such as neurotoxicity and neurological disorder, eye damage, cardiovascular injury, liver injury, and energy metabolism disorder. In addition, this review briefly discusses with special attention to the strategies for developing potential therapies by future applications of these medicinal plants and bioactive compounds, which will help biological and pharmacological scientists to explore the new vistas of medicinal plants in combating 4-HNE-induced deleterious effects.

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Cyanidin-3-glucoside Alleviates 4-Hydroxyhexenal-Induced NLRP3 Inflammasome Activation via JNK-c-Jun/AP-1 Pathway in Human Retinal Pigment Epithelial Cells

Cited by 34 publications

References 44 publications

Down-regulation of RalGTPase-Activating Protein Promotes Colitis-Associated Cancer via NLRP3 Inflammasome Activation

Down-regulation of RalGTPase-Activating Protein Promotes Colitis-Associated Cancer via NLRP3 Inflammasome Activation

NOD-like Receptors in the Eye: Uncovering Its Role in Diabetic Retinopathy

Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

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