Korean red ginseng extracts inhibit NLRP3 and AIM2 inflammasome activation

Kim, Jee Young; Ahn, Huijeong; Han, Byung-Cheol; Lee, Seungho; Cho, Young Wook; Kim, Cheon Ho; Hong, Eui‐Ju; An, Beum‐Soo; Jeung, Eui‐Bae; Lee, Geun‐Shik

doi:10.1016/j.imlet.2013.12.017

Cited by 66 publications

(66 citation statements)

References 45 publications

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“…[84] showed that ginseng saponins reduced the production of pro-inflammatory cytokines such as TNF-α and IL-1β, suggesting that the saponins (pfaffosides) in the extract may be responsible for these effects. Furthermore, in a mouse model of intestinal inflammation, phytosterols, such as β-sitosterol, which has a number of beneficial effects in inflammatory models, decreased the activity of colonic MPO by 28% and the expression of IL-1β, TNF-α, and IL-6 [85].…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of Brazilian ginseng (Pfaffia paniculata) on TNBS-induced intestinal inflammation: Experimental evidence

Costa

Tanimoto

Quaglio

et al. 2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of Brazilian ginseng (Pfaffia paniculata) on TNBS-induced intestinal inflammation: Experimental evidence

Costa

Tanimoto

Quaglio

et al. 2015

International Immunopharmacology

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“…P. ginseng suppressed IL-1β maturation by suppressing the activation of NLRP3 inflammasome in macrophages as well as the murine model [8] . In addition, P. ginseng strongly attenuated IL-1β secretion by inhibiting AIM2 inflammasome activation, suggesting that P. ginseng could act as a potential modulator of the inflammasome complex [8] .…”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 97%

“…In addition, igongsan, which is another compound from ginseng, showed inhibitory effects against caspase-1 activity, resulting in the inhibition of inflammation [7] . Moreover, activation of IL-1β is regulated by inflammasome, which includes NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome, interferon-inducible protein AIM2 inflammasome, and NLRC4 (NLR Family, CARD domain-containing 4) inflammasome [8] . P. ginseng suppressed IL-1β maturation by suppressing the activation of NLRP3 inflammasome in macrophages as well as the murine model [8] .…”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

“…Moreover, activation of IL-1β is regulated by inflammasome, which includes NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome, interferon-inducible protein AIM2 inflammasome, and NLRC4 (NLR Family, CARD domain-containing 4) inflammasome [8] . P. ginseng suppressed IL-1β maturation by suppressing the activation of NLRP3 inflammasome in macrophages as well as the murine model [8] . In addition, P. ginseng strongly attenuated IL-1β secretion by inhibiting AIM2 inflammasome activation, suggesting that P. ginseng could act as a potential modulator of the inflammasome complex [8] .…”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

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Panax ginseng as a potential modulator of macrophages

Nguyen¹,

Rhee

2016

Macrophage

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Bacteria-induced sepsis is a medical emergency requiring immediate intervention; the key to prevent sepsis is to prevent an infection from occurring in the first place. Although Panax ginseng (Korean ginseng) has been well known as an immune modulator, its role in bacterial sepsis is not well understood. Using RAW 264.7 macrophages and a murine model, we elucidated the protective effect of P. ginseng against community-associated Streptococcus pneumoniae (pneumococcus)-induced sepsis via inhibition of inflammation. In pneumococcal infections, pre-treatment with P. ginseng decreased the expressions of Toll-like receptor 4 (TLR4) and tumor necrosis factor (TNF)-ɑ in RAW 264.7 macrophages, but increased the expression of phosphoinositide 3-kinase (PI3K) and AKT kinase, thereby enhancing cellular viability. Furthermore, secretion of pro-inflammatory cytokines (TNF-ɑ and interleukin (IL)-1β) as well as neutrophil infiltration was diminished by pre-treatment with P. ginseng. As a result, mice pre-treated with P. ginseng demonstrated significantly higher survival rate and body weight gain than the non-treated mice (control). Treated mice showed diminished colonization of bacteria and morbidity. In addition, some studies have indicated that P. ginseng or ginseng compounds activated macrophage functions, which supports the immune system against cancer and other diseases. In the present study, we will discuss dual roles of P. ginseng in modulating macrophage functions.

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“…Mechanistically, these effects may all derive from the findings that red ginseng can block LPS-induced expression of NO, PGE2, COX2, TNFα, and IL-6 in cell lines, presumably through inhibition of NFκB nuclear translocation. 147 There is also very recent evidence that red ginseng inhibits the NLRP3 (and possibly AIM2) inflammasome, 148 resulting in reduced IL-1β production. Taken together, these results suggest a clear effect of ginseng on the pain pathway and a need for future clinical studies examining the efficacy of ginseng as a natural antiinflammatory.…”

Section: Ginsengmentioning

confidence: 99%