Effects of ginsenoside Re on LPS-induced inflammatory mediators in BV2 microglial cells

Lee, Kang-Woo; Jung, So Young; Choi, Sun-Mi; Yang, Eun Jin

doi:10.1186/1472-6882-12-196

Cited by 65 publications

(43 citation statements)

References 35 publications

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“…Excessive inflammation plays a pivotal role in the pathogenesis of organ injury, especially in the heart. LPS is widely used to induce inflammation response, as evaluated by increase of pro-inflammatory cytokines (Lee et al, 2012a). What is more, MMPs, which is increased upon exposure to LPS, can provoke inflammatory signaling in remodeling process (DeLeon-Pennell et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Xianchu¹,

Zheng²,

Liu³

et al. 2018

J. Toxicol. Sci.

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Rutin has a wide range of beneficial health properties in the amelioration of multi-organ injury owing to its various biological effects. The aim of this study was to investigate the effects of rutin on lipopolysaccharide (LPS)-induced heart injury and clarify its potential cardioprotective mechanism. The mouse model of heart injury was intraperitoneal infection with LPS, and rutin was orally administered for 8 consecutive days. One day after LPS injection, heart histopathology, cardiac marker enzymes and cardiac fibrosis related genes were determined to evaluate the cardioprotective effects of rutin. In addition, oxidative parameters and inflammatory cytokines were tested to explore its possible underlying mechanism. The presented results showed that rutin significantly improved morphological changes of myocardium and relieved cardiac marker enzymes [creatine kinase (CK) and lactate dehydrogenase (LDH)] level to protect heart in LPS-induced sepsis. And more, rutin observably mitigated fibrosis related genes [matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9)] expression in the heart to prevent against LPS-induced cardiac fibrosis. In addition, rutin markedly increased antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] activity, and improved oxidative production [malondialdehyde (MDA) and HO] level to balance the oxidation and anti-oxidation systems in the heart. Lastly, rutin dramatically ameliorated [tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6)] activity to restrain inflammatory responses in the heart. In conclusion, rutin possessed anti-oxidant and anti-inflammatory properties to improve LPS-induced heart injury, which suggested rutin could be used as a potential cardioprotective medicine in sepsis.

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Section: Discussionmentioning

confidence: 99%

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Xianchu¹,

Zheng²,

Liu³

et al. 2018

J. Toxicol. Sci.

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“…Among ginsenosides, ginsenoside Re, Rd, and Rg1 are known to be mainly present in the ginseng leaves (Kim et al 2015). Lee et al have showed that ginsenoside Re may lead to an anti-neuro inflammatory effect on p38 signaling in LPS-induced BV2 microglial cells (Lee et al 2012). Moreover, Wu et al indicated that the divergent structure of the ginsenosides including Re, Rd, and Rg1, are responsible for the anti-inflammatory effects in LPS-induced N9 microglial cells by blocking NF-jB signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Gold nanoparticles synthesized using Panax ginseng leaves suppress inflammatory - mediators production via blockade of NF-κB activation in macrophages

Ahn

Singh

Castro-Aceituno

et al. 2016

Artificial Cells, Nanomedicine, and Biotechnology

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In the present study, we report that Gold nanoparticles (AuNPs) synthesized using the leaf extract of Panax ginseng Meyer (P.g AuNPs) exert anti-inflammatory effects through inhibition of downstream NF-κB activation in macrophages. We found that P.g AuNPs reduced the expression of the inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PEG), interleukin (IL)-6, tumor necrosis factor-α (TNF-α) was attenuated by P.g AuNPs. Furthermore, P.g AuNPs suppressed lipopolysaccharide (LPS)-induced activation of NF-κB signaling pathway via p38 mitogen-activated protein kinase (MAPK) in RAW 264.7 cells. Taken together, our results suggest that P.g AuNPs can be utilized as a novel therapeutic agent for the prevention and cure of inflammation.

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“…These ginsenosides have been reported to show various biological activities, including anti-inflammatory activity. Commonly studied ginsenosides such as both protopanaxatriol-type ginsenosides Rg1, Re and protopanaxadiol-type ginsenosides Rb2, Rd demonstrate anti-inflammatory effects [19, 20]. Recently, results have shown that compound K transformed from Rb2 is effective against inflammation [21].…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rh2 Downregulates LPS-Induced NF-κB Activation through Inhibition of TAK1 Phosphorylation in RAW 264.7 Murine Macrophage

Lian

Jin

Shen

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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The present study was carried out to evaluate the inhibitory effects of ginsenoside Rh2 on nuclear-factor- (NF-) κB in lipopolysaccharide- (LPS-) activated RAW 264.7 murine macrophages. RAW 264.7 cells were pretreated with indicated concentrations of ginsenoside Rh2 for 1 h prior to the incubation of LPS (1 μg/mL) for indicated time period. Ginsenoside Rh2 reduced CD14 and Toll-like receptor 4 (TLR4) expressions 24 h after LPS stimulation. Furthermore, ginsenoside Rh2 significantly inhibited TGF-beta-activated kinase 1 (TAK1) phosphorylation 30 min after LPS stimulation. Ginsenoside Rh2 was further shown to inhibit NF-κB p65 translocation into the nucleus by suppressing IκB-α degradation. Also, LPS increased mRNA expression of TNF-α and IL-1α time-dependently, while TQ reduced TNF-α within 3 h and IL-1α within 1 h. And we firstly found that pretreatment of ginsenoside Rh2 successively inhibited hypoxia-inducible factor- (HIF-) 1α expression increased by LPS. In conclusion, ginsenoside Rh2 may inhibit LPS-induced NF-κB activation and reduce HIF-1α accumulation, suggesting that ginsenoside Rh2 may be considered as a potential therapeutic candidate for chronic inflammatory diseases.

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Effects of ginsenoside Re on LPS-induced inflammatory mediators in BV2 microglial cells

Cited by 65 publications

References 35 publications

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Protective effects of rutin on lipopolysaccharide-induced heart injury in mice

Gold nanoparticles synthesized using Panax ginseng leaves suppress inflammatory - mediators production via blockade of NF-κB activation in macrophages

Ginsenoside Rh2 Downregulates LPS-Induced NF-κB Activation through Inhibition of TAK1 Phosphorylation in RAW 264.7 Murine Macrophage

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