Anti‐Inflammatory Activity of Rg3‐Enriched Korean Red Ginseng Extract in Murine Model of Sepsis

Abstract

Ginseng has therapeutic effects on various bodily disorders ranging from minor inflammation to major cardiovascular diseases. In our study, we explored the anti-inflammatory effects of Rg3-enriched red ginseng extract (Rg3-RGE), a ginsenoside belonging to the panaxadiol group. We employed nitric oxide assay (NO) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), western blot, and hematoxylin and eosin staining (H&E) to elucidate the anti-inflammatory activity of Rg3-RGE. Rg3-RGE potently suppressed NO production in the murine macrophage cell line, RAW 264.7 cells, without any cytotoxicity across dosages. Additionally, it inhibited the mRNA expression of proinflammatory mediators and cytokines like iNOS, COX-2, IL-1β, IL-6, and TNF-α. Moreover it also inhibited the levels of malondialdehyde levels in serum of septic shock mice. Immunoblot analysis showed that Rg3-RGE induced anti-inflammatory signal transduction via the NF-κB and MAPK pathways. A remarkable attenuation of inflammation by oral treatment with Rg3-RGE in mice was observed in the survival study. The in vivo study using a septic shock mouse model also showed similar results as the in vitro study. Our findings suggest that Rg3-RGE can potentially be a potent anti-inflammatory agent that likely mediates its anti-inflammatory effects via the NF-κB and MAPK pathways.

Alleviation of Ulcerative Colitis Potentially through th1/th2 Cytokine Balance by a Mixture of Rg3-enriched Korean Red Ginseng Extract and Persicaria tinctoria

“…We have previously reported the anti-inflammatory effects of Rg3-RGE [ 29 ], where mice induced with sepsis have been rescued. In that study, we have shown that Rg3-RGE has potently inhibited pro-inflammatory mediators and cytokines, and suppressed proteins in the NF-κB and MAPK pathway.…”

Pro-Resolving Effect of Ginsenosides as an Anti-Inflammatory Mechanism of Panax ginseng

“…Ginsenoside Rg3-enriched red ginseng extract potently suppressed NO production in murine RAW 264.7 macrophages, without any cytotoxicity across dosages. Additionally, it inhibited the mRNA expression of pro-inflammatory mediators and cytokines such as iNOS, COX-2, IL-1β, IL-6, and TNF-α [58]. Therefore, ginsenoside Rg3 was reported as an anti-inflammatory constituent in M1-polarized macrophages and in vivo conditions.…”

Effects of Ginsenoside Rg3 on Inhibiting Differentiation, Adipogenesis, and ER Stress-Mediated Cell Death in Brown Adipocytes

“…Recent evidence has shown that natural compound derivatives such as paclitaxel, doxorubicin, and artemisinin have therapeutic efficacies for various diseases, including tumors and malaria [4,6,20]. Rg3, an important natural compound in Korean red ginseng (Panax ginseng) [8], has demonstrated significant therapeutic effects, including inhibition of cancer progression, prevention of platelet aggregation, regulation of neurotransmitters, attenuation of inflammatory cytokines, and modulation of vascular tones [10][11][12][13]. Rg3 also has inhibitory effects on the adipogenic properties of mouse and human white preadipocytes [14], although little is known about its effects on brown preadipocytes or differentiated brown adipocytes.…”

“…Ginsenoside Rg3 (Rg3), which is a major bioactive component of Korean red ginseng ( Panax ginseng ) [ 8 ], possesses various therapeutic benefits such as anticancer effects against various malignant cells [ 9 ], inhibition of platelet aggregation [ 10 ], antidepressant effects mediated via regulation of neurotransmitters [ 11 ], reduction of proinflammatory cytokines [ 12 ], and modulation of vascular functions [ 13 ]. Rg3 has also been shown to inhibit cell differentiation and viability of 3T3-L1 preadipocytes and reduce expression of adipogenic markers such as peroxisome proliferator-activated receptor gamma (PPAR γ ) and CCAAT/enhancer binding protein alpha (C/EBP α ) in livers of obese mice [ 14 ].…”