Protective effect of saponins extract from<i>Panax japonicus</i>on myocardial infarction: involvement of NF-κB, Sirt1 and mitogen-activated protein kinase signalling pathways and inhibition of inflammation

Wei, Na; Zhang, Changcheng; He, Hui; Wang, Ting; Liu, Zhaoqi; Liu, Guangyao; Sun, Zhiwei; Zhou, Zhi; Bai, Cai-hong; Yuan, Ding

doi:10.1111/jphp.12291

Cited by 37 publications

(19 citation statements)

References 45 publications

(88 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been known that MAPK signaling pathways play critical roles in the regulation of inflammatory mediators [34,35]. Especially, ERK1/2 and p38 MAPK signaling pathways serve as main signaling pathways in inflammatory response [18,19]. It has been reported that stimulating of RAW264.7 by LPS induces phosphorylation and activation of ERK1/2 and p38 MAPKs [11,36].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hyperin attenuates inflammation by activating PPAR-γ in mice with acute liver injury (ALI) and LPS-induced RAW264.7 cells

Huang

Yang

et al. 2015

International Immunopharmacology

View full text Add to dashboard Cite

Hyperin (HP) is a flavonoid compound found in various plants like Ericaceae, Guttifera and Celastraceae. The present study has revealed that HP has a variety of pharmacological effects including anti-oxidant, anticancer, and anti-coagulant, especially anti-inflammatory. However, the potential molecular mechanism of anti-inflammatory is still unrevealed. In this study, HP not only significantly attenuated inflammation in C57BL/6J mice with acute liver injury (ALI), but also reduced the expression of TNF-α and IL-6 in lipopolysaccharide (LPS)-induced RAW264.7 cells. Furthermore, our findings showed that HP remarkably induced the expression of PPAR-γ in vivo and in vitro. Interestingly, compared with the HP treatment group, a specific blocking agent of PPAR-γ T0070907 and PPAR-γ small interfering (si)-RNA-mediated silencing in RAW264.7 cells were used to evaluate the involvement of HP in alleviating LPS-induced inflammation. More importantly, over-expression of PPAR-γ had an opposite effect on the expression of TNF-α and IL-6 in LPS-induced RAW264.7 cells after treatment with HP. In addition, HP remarkably inhibited the expression of P-ERK1/2 and P-P38 MAPK. Taken together, all the above results indicate that HP may serve as an effective modulator of PPAR-γ, further down-regulating ERK1/2 and p38 MAPK during the pathogenesis of inflammation.

show abstract

Section: Discussionmentioning

confidence: 99%

“…It has been reported that MAPK is involved in the regulation of inflammatory mediator production, especially P-ERK1/2 and P-P38 MAPK activities [18,19]. Thus, the effect of HP on P-ERK1/2 and P-P38 expression in vivo and in vitro was investigated.…”

Section: Hp Suppresses P-erk1/2 and P-p38 Expression In Vivo And In Vmentioning

confidence: 99%

Hyperin attenuates inflammation by activating PPAR-γ in mice with acute liver injury (ALI) and LPS-induced RAW264.7 cells

Huang

Yang

et al. 2015

International Immunopharmacology

View full text Add to dashboard Cite

show abstract

“…However, the clinical application of MSC transplantation is restricted by low survival rates of MSCs following transplantation (6). Several signaling pathways are abnormally regulated in the process of MI, including transforming growth factor-β (TGF-β)/small mothers against decapentaplegic, Janus kinase-signal transducers and activators of transcription, p38 mitogen-activated protein kinases (p38MAPK), phosphoinositide-3-kinase (PI3K)/Akt-endothelial nitric oxide synthase, PI3K/protein kinase C and Wnt (7)(8)(9). Among these signaling pathways, p38MAPK is involved in regulating the inflammatory process.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of p38MAPK potentiates mesenchymal stem cell therapy against myocardial infarction injury in rats

Zhang

Zhou

Mei

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

The present study aimed to investigate the protective effect of mesenchymal stem cell (MSC) therapy in combination with p38 mitogen‑activated protein (MAPK) inhibition against myocardial infarction (MI) injury in rats, and to elucidate the underlying mechanisms. An MI model was established by ligation of the anterior descending branch of the left coronary artery. The rats were divided into four groups: MSC transplantation, p38MAPK inhibitor (SB203580), MSC + SB203580 and model control group. HE staining and a TUNEL assay were performed to evaluate pathological changes and apoptosis. The expression levels of p38MAPK and transforming growth factor β‑activated kinase 1 (TAK1) were determined using reverse transcription‑polymerase chain reaction and western blot analyses. As shown by HE staining, classical morphological changes, including irregular cell arrangement and inflammatory infiltration were observed in the model rats, whereas MSC therapy or injection of the p38MAPK inhibitor ameliorated these pathological changes. Of note, the combined application of MSCs with the p38MAPK inhibitor exerted additive effects. The TUNEL assay showed that the combined application of MSCs with p38MAPK inhibitor also led to potentiation of effects, compared with either MSCs therapy or p38MAPK inhibitor injection alone. Mechanistically, the combined application of MSCs with p38MAPK inhibitor decreased the expression levels of TAK1 and p38MAPK at the mRNA and protein levels. In conclusion, p38MAPK inhibition potentiated the protective effects of MSCs therapy against MI in rats.

show abstract

“…This study also showed that the benefit could be enhanced with coadministration of extracts of the Safflower plant (Cartharmus tinctorius L) thus suggesting that combination therapy could effectively enhance the cardioprotective effect of ginseng-related compounds. Furthermore, seven-day pretreatment with a saponin extract from P japonicas exerted substantial protection in rats subjected to 12 hours of coronary artery ligation, without reperfusion, as manifested by improved function, reduced injury including apoptosis as well as reduced markers of oxidative stress and expression levels of cytokines (He et al 2012;Wei et al 2014).…”

Section: R a F Tmentioning

confidence: 98%

Cardioprotection by ginseng: experimental and clinical evidence and underlying mechanisms

Gan

Karmazyn

2018

Can. J. Physiol. Pharmacol.

View full text Add to dashboard Cite

Protection of the ischemic and reperfused myocardium represents a major therapeutic challenge. Translating results from animal studies to the clinical setting has been disappointing, yet the need for effective intervention, particularly to limit heart damage following infarction or surgical procedures such as coronary artery bypass grafting, is substantial. Among the many compounds touted as cardioprotective agents is ginseng, a medicinal herb belonging to the genus Panax, which has been used as a medicinal agent for thousands of years, particularly in Asian societies. The biological actions of ginseng are very complex and reflect composition of many bioactive components, although many of the biological and therapeutic effects of ginseng have been attributed to the presence of steroid-like saponins termed ginsenosides. Both ginseng and many ginsenosides have been shown to exert cardioprotective properties in experimental models. There is also clinical evidence that traditional Chinese medications containing ginseng exert cardioprotective properties, although such clinical evidence is less robust primarily owing to the paucity of large-scale clinical trials. Here, we discuss the experimental and clinical evidence for ginseng, ginsenosides, and ginseng-containing formulations as cardioprotective agents against ischemic and reperfusion injury. We further discuss potential mechanisms, particularly as these relate to antioxidant properties.

show abstract

Protective effect of saponins extract fromPanax japonicuson myocardial infarction: involvement of NF-κB, Sirt1 and mitogen-activated protein kinase signalling pathways and inhibition of inflammation

Abstract: The studies demonstrated that SPJ exerted beneficially cardioprotective effects on MI rats, mainly inhibiting NF-κB, ERK1/2 and p38 MAPK activation, but increased the expression of SIRT1, alleviating MI injury and cardiac cell death.

Cited by 37 publications

References 45 publications

Hyperin attenuates inflammation by activating PPAR-γ in mice with acute liver injury (ALI) and LPS-induced RAW264.7 cells

Hyperin attenuates inflammation by activating PPAR-γ in mice with acute liver injury (ALI) and LPS-induced RAW264.7 cells

Inhibition of p38MAPK potentiates mesenchymal stem cell therapy against myocardial infarction injury in rats

Cardioprotection by ginseng: experimental and clinical evidence and underlying mechanisms

Contact Info

Product

Resources

About