Ginsenoside Rd alleviates mouse acute renal ischemia/reperfusion injury by modulating macrophage phenotype

Ren, Kaixi; Jin, Chao; Ma, Ping; Ren, Qin-You; Jia, Zhansheng; Zhu, Daocheng

doi:10.1016/j.jgr.2015.12.003

Cited by 32 publications

(15 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ginsenosides such as Rd and Rb1 have been reported to affect macrophage polarization and atherosclerosis progression; however, there has been no related research on diabetic atherosclerosis ( Ren et al, 2016 ; Zhang et al, 2017 ). This report revealed that 20(S)-Rg3 could reduce the plaque burden and enhance plaque stability in diabetic mice, the effects of which were mostly achieved by suppressing AGEs-induced M1 macrophage activation and promoting M2 macrophage polarization via PPARγ activation ( Figure 8 ).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 Mitigates Atherosclerosis Progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype

et al. 2018

View full text Add to dashboard Cite

Atherosclerosis (AS) in diabetic patients is often associated with low stability, which might be largely attributed to unfavorable macrophage polarization and increased inflammatory response induced by hyperglycaemia. Ginsenoside Rg3 is one of the main active principles of Panax Ginseng, which has been reported to be a natural ligand of peroxisome proliferator-activated receptor-gamma (PPARγ), a key nuclear transcriptional factor involved in inflammation and macrophage differentiation. However, it remains unclear if Rg3 could exert protective effects on plaque stability in diabetes. In this study, we investigated the role of ginsenoside 20(S)-Rg3 in macrophage polarization and AS plaque stability using advanced glycation end products-treated macrophages and diabetic AS mice models. In vitro, advanced glycation end products (AGEs) treatment promoted the expression of proinflammatory molecules and M1 surface markers, whereas 20(S)-Rg3 could reverse the M1 polarization to the M2 phenotype. In vivo, the administration of 20(S)-Rg3 promoted AS lesion stability and reduced the plaque burden, accompanied by increased M2 macrophages and reduced M1 macrophages. In addition, PPARγ antagonist GW9662 co-administration mostly blocked these effects, suggesting the important role of PPARγ pathways in mediating 20(S)-Rg3 effects in macrophage polarization and atherosclerosis progression. Together, these results demonstrated an immunomodulatory role of ginsenoside 20(S)-Rg3 in promoting macrophages to a profile of the M2 type through PPARγ-dependent mechanisms, and indicated a potential role of 20(S)-Rg3 in the prevention and treatment of diabetic atherosclerosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 Mitigates Atherosclerosis Progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Inflammatory cells, such as macrophages and neutrophils, let leukocytes and plasma components come to sites where infection or injury has occurred during inflammation to eliminate dangers (Nowarski et al 2013;Lee et al 2016). Although inflammation is important to the immune system, excessive activity of inflammatory cells can cause cancer, rheumatoid arthritis, multiple sclerosis, chronic asthma, psoriasis, and other diseases (Gautam and Jachak 2009;Nowarski et al 2013;Ren et al 2016). To treat those inflammation-driven diseases, inflammatory responses should be controlled.…”

Section: Introductionmentioning

confidence: 99%

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Berköz

2019

gpb

View full text Add to dashboard Cite

Diosmin is an unsaturated flavonoid glycoside, presents in citrus fruits. The aim of this study is to investigate the molecular mechanism of diosmin with respect to the NF-κB and MAPKs signaling pathways. Firstly, 10, 20, 30, 40 and 50 µM diosmin were treated to lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. The anti-inflammatory effects of diosmin was displayed via measuring prostaglandin E 2 (PGE 2), nitric oxide (NO), interleukines (IL-6, IL-12), tumor necrosis factor α (TNF-α) production, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), IL-6, IL-12, TNF-α mRNA levels, and phosphorylation levels of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκB-α) and mitogen-activated protein kinases (MAPKs); JNK, ERK, and p38 in LPS induced RAW264.7 macrophages. Our study showed that especially high concentrations of diosmin decreased NO, PGE 2 , IL-6, IL-12, TNF-α production and mRNA levels of these mediators (p < 0.05). The expression of phosphorylated-JNK was significantly suppressed by diosmin at 40 and 50 µM concentrations. Furthermore, diosmin significantly inhibited the expression of phosphorylated-ERK, p38, and p-IκB-α in a dose-dependent manner. Our results suggest that diosmin is a potent anti-inflammatory agent and has potential for development into a therapeutic agent for inflammation-associated disorders.

show abstract

“…Inflammatory cells, such as macrophages and neutrophils, let leukocytes and plasma components come to sites where infection or injury has occurred during inflammation to eliminate dangers [ 1 , 2 ]. Although inflammation is important to the immune system, excessive activity of inflammatory cells can cause cancer, rheumatoid arthritis, multiple sclerosis, chronic asthma, psoriasis, and other diseases [ 1 , 3 , 4 ]. To treat those inflammation-driven diseases, inflammatory responses should be controlled.…”

Section: Introductionmentioning

confidence: 99%

Anti‐Inflammatory Effect of Piper attenuatum Methanol Extract in LPS‐Stimulated Inflammatory Responses

Kim

Jeong

Kim

et al. 2017

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Piper attenuatum is used as a traditional medicinal plant in India. One of the substances in P. attenuatum has been suggested to have anti-inflammatory effects. However, there is insufficient research about the anti-inflammatory mechanisms of action of P. attenuatum. The effects of P. attenuatum methanol extract (Pa-ME) on the production of inflammatory mediators nitric oxide (NO) and prostaglandin E2 (PGE2), the expression of proinflammatory genes, the translocation level of transcription factors, and intracellular signaling activities were investigated using macrophages. Pa-ME suppressed the production of NO and PGE2 in lipopolysaccharide- (LPS-), pam3CSK4-, and poly(I:C)-stimulated RAW264.7 cells without displaying cytotoxicity. The mRNA expression levels of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2) were decreased by Pa-ME. P-ME reduced the translocation of p50/NF-κB and AP-1 (c-Jun and c-Fos), as well as the activity of their upstream enzymes Src, Syk, and TAK1. Immunoprecipitation analysis showed failure of binding between their substrates, phospho- (p-) p85 and p-MKK3/6. p-p85 and p-MKK3/6, which were induced by overexpression of Src, Syk, and TAK1, were also reduced by Pa-ME. Therefore, these results suggest that Pa-ME exerts its anti-inflammatory effects by targeting Src and Syk in the NF-κB signaling pathway and TAK1 in the AP-1 signaling pathway.

show abstract

Ginsenoside Rd alleviates mouse acute renal ischemia/reperfusion injury by modulating macrophage phenotype

Cited by 32 publications

References 30 publications

Ginsenoside Rg3 Mitigates Atherosclerosis Progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype

Ginsenoside Rg3 Mitigates Atherosclerosis Progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Anti‐Inflammatory Effect of Piper attenuatum Methanol Extract in LPS‐Stimulated Inflammatory Responses

Contact Info

Product

Resources

About