Ginsenoside Rg3 regulates S-nitrosylation of the NLRP3 inflammasome via suppression of iNOS

Yoon, SungJin; Park, Jun-Young; Choi, Song Hee; Lee, Jin-Bong; Jung, Hye Young; Kim, Tae-Don; Yoon, Suk Ran; Choi, Inpyo; Shim, Sungbo; Park, Young-Jun

doi:10.1016/j.bbrc.2015.06.080

Cited by 81 publications

(62 citation statements)

References 24 publications

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“…Ginsenoside Rg3 has been shown to enhance the radiosensitivity of human esophageal carcinoma cells by downregulating the expression of VEGF and hypoxia inducible factor-1α (6), and ginsenoside Rg3 may have a neuroprotective function in the rat hippocampus via the inhibition of hippocampus-mediated N-methyl-D-aspartate receptor activation (7). Additional biological activities associated with gene regulation have also been demonstrated for this molecule (2,8). …”

Section: Introductionmentioning

confidence: 92%

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Teng

Wang

et al. 2017

Molecular Medicine Reports

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Ginsenoside Rg3, a bioactive constituent isolated from Panax ginseng, exhibits antitumorigenic, antioxidative, antiangiogenic, neuroprotective and other biological activities are associated with the regulation of multiple genes. DNA methylation patterns, particularly those in the promoter region, affect gene expression, and DNA methylation is catalyzed by DNA methylases. However, whether ginsenoside Rg3 affects DNA methylation is unknown. High performance liquid chromatography assay, MspI/HpaII polymerase chain reaction (PCR) and reverse transcription-quantitative PCR were performed to assess DNA methylation. It was demonstrated that 20(S)-ginsenoside Rg3 treatment resulted in increased inhibition of cell growth, compared with treatment with 20(R)-ginsenoside Rg3 in the human HepG2 hepatocarcinoma cell line. It was additionally revealed that treatment with 20(S)-ginsenoside Rg3 reduced global genomic DNA methylation, altered cystosine methylation of the promoter regions of P53, B cell lymphoma 2 and vascular endothelial growth factor, and downregulated the expression of DNA methyltransferase (DNMT) 3a and DNMT3b more than treatment with 20(R)-ginsenoside Rg3 in HepG2 cells. These results revealed that the modulation of DNA methylation may be important in the pharmaceutical activities of ginsenoside Rg3.

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Section: Introductionmentioning

confidence: 92%

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Teng

Wang

et al. 2017

Molecular Medicine Reports

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“…Interestingly, a group of naturally occurring compounds, ginsenosides, were shown to reduce S -nitrosylation of NLRP3 by reducing iNOS expression. 190 This was proposed as a mechanism by which ginsenosides can protect against LPS-induced endotoxic shock.…”

Section: Other Post-translational Modifications Of Nlrp3mentioning

confidence: 99%

Post-translational regulation of inflammasomes

2016

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Inflammasomes play essential roles in immune protection against microbial infections. However, excessive inflammation is implicated in various human diseases, including autoinflammatory syndromes, diabetes, multiple sclerosis, cardiovascular disorders and neurodegenerative diseases. Therefore, precise regulation of inflammasome activities is critical for adequate immune protection while limiting collateral tissue damage. In this review, we focus on the emerging roles of post-translational modifications (PTMs) that regulate activation of the NLRP3, NLRP1, NLRC4, AIM2 and IFI16 inflammasomes. We anticipate that these types of PTMs will be identified in other types of and less well-characterized inflammasomes. Because these highly diverse and versatile PTMs shape distinct inflammatory responses in response to infections and tissue damage, targeting the enzymes involved in these PTMs will undoubtedly offer opportunities for precise modulation of inflammasome activities under various pathophysiological conditions.

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“…UVB and LL-37-induced P2X7 receptor activation increased intracellular calcium concentrations, which triggered inflammasome activation and IL-1β release [44]. Using Ginsenoside Rg3 (the major bioactive ingredient of Panax ginseng) as an antioxidant to regulate inflammasome can block nitric oxide (NO) production and thus decrease the NLRP3 inflammasome in macrophage and HaCaT cells following UVB exposure [46]. It has been shown that ROS are involved in UVB-induced activation of the NLRP3 inflammasome [46].…”

Section: The Possible Role Of the Inflammasome And Autophagy In Uvmentioning

confidence: 99%

“…Using Ginsenoside Rg3 (the major bioactive ingredient of Panax ginseng) as an antioxidant to regulate inflammasome can block nitric oxide (NO) production and thus decrease the NLRP3 inflammasome in macrophage and HaCaT cells following UVB exposure [46]. It has been shown that ROS are involved in UVB-induced activation of the NLRP3 inflammasome [46]. Clearly, much remains to be learned about the mechanisms of inflammasome activation and its pathophysiological consequences in the context of UVR-induced skin damage.…”

Section: The Possible Role Of the Inflammasome And Autophagy In Uvmentioning

confidence: 99%

The Roles of Autophagy and the Inflammasome during Environmental Stress-Triggered Skin Inflammation

Chen

Lee

Yeh

et al. 2016

IJMS

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Inflammatory skin diseases are the most common problem in dermatology. The induction of skin inflammation by environmental stressors such as ultraviolet radiation (UVR), hexavalent chromium (Cr(VI)) and TiO2/ZnO/Ag nanoparticles (NPs) has been demonstrated previously. Recent studies have indicated that the inflammasome is often wrongly activated by these environmental irritants, thus inducing massive inflammation and resulting in the development of inflammatory diseases. The regulation of the inflammasome with respect to skin inflammation is complex and is still not completely understood. Autophagy, an intracellular degradation system that is associated with the maintenance of cellular homeostasis, plays a key role in inflammasome inactivation. As a housekeeping pathway, cells utilize autophagy to maintain the homeostasis of the organ structure and function when exposed to environmental stressors. However, only a few studies have examined the effect of autophagy and/or the inflammasome on skin pathogenesis. Here we review recent findings regarding the involvement of autophagy and inflammasome activation during skin inflammation. We posit that autophagy induction is a novel mechanism inter-modulating environmental stressor-induced skin inflammation. We also attempt to highlight the role of the inflammasome and the possible underlying mechanisms and pathways reflecting the pathogenesis of skin inflammation induced by UVR, Cr(VI) and TiO2/ZnO/Ag NPs. A more profound understanding about the crosstalk between autophagy and the inflammasome will contribute to the development of prevention and intervention strategies against human skin disease.

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Ginsenoside Rg3 regulates S-nitrosylation of the NLRP3 inflammasome via suppression of iNOS

Cited by 81 publications

References 24 publications

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Effects of R type and S type ginsenoside Rg3 on DNA methylation in human hepatocarcinoma cells

Post-translational regulation of inflammasomes

The Roles of Autophagy and the Inflammasome during Environmental Stress-Triggered Skin Inflammation

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