Water-soluble andrographolide sulfonate exerts anti-sepsis action in mice through down-regulating p38 MAPK, STAT3 and NF-κB pathways

Guo, Wenjie; Li, Wen; Chen, Gong; Hong, Shaocheng; Cheng, Qi; Xie, Ning; Yang, Xiaoling; Sun, Yang; Xu, Qiang

doi:10.1016/j.intimp.2012.09.002

Cited by 62 publications

(36 citation statements)

References 34 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Briefly, upstream signals lead to phosphorylation and ubiquitin-dependent degradation of I κ B α or I κ B β and translocation of p65-related dimmers into the nucleus followed by subsequent gene transcription. There also are reports that ERK1/2 [29–31] and STAT3 [32, 33] as upstream regulator participating in the activation of NF- κ B signaling pathway in sepsis. We therefore further explored the effect of CB2R activation on the LPS/TLR4 signal pathway.…”

Section: Resultsmentioning

confidence: 99%

Cannabinoid Receptor 2 Protects against Acute Experimental Sepsis in Mice

Gui

Sun

Luo

et al. 2013

Mediators of Inflammation

Self Cite

View full text Add to dashboard Cite

The systemic inflammatory response syndrome can be self-limited or can progress to severe sepsis and septic shock. Despite significant advances in the understanding of the molecular and cellular mechanisms of septic shock, it is still one of the most frequent and serious problems confronting clinicians in the treatments. And the effects of cannabinoid receptor 2 (CB2R) on the sepsis still remain undefined. The present study was aimed to explore the role and mechanism of CB2R in acute sepsis model of mice. Here, we found that mice were more vulnerable for lipopolysaccharide- (LPS-) induced death and inflammation after CB2R deletion (CB2R−/−). CB2R agonist, GW405833, could significantly extend the survival rate and decrease serum proinflammatory cytokines in LPS-treated mice. GW405833 dose-dependently inhibits proinflammatory cytokines release in splenocytes and peritoneal macrophages as well as splenocytes proliferation, and these effects were partly abolished in CB2R−/− splenocytes but completely abolished in CB2R−/− peritoneal macrophages. Further studies showed that GW405833 inhibits LPS-induced phosphorylation of ERK1/2 and STAT3 and blocks IκBα degradation and NF-κB p65 nuclear translocation in macrophages. All data together showed that CB2R provides a protection and is a potential therapeutic target for the sepsis.

show abstract

Section: Resultsmentioning

confidence: 99%

Cannabinoid Receptor 2 Protects against Acute Experimental Sepsis in Mice

Gui

Sun

Luo

et al. 2013

Mediators of Inflammation

Self Cite

View full text Add to dashboard Cite

show abstract

“…Stumpf et al (46) reported that DS and its major ingredients significantly inhibited TNF-α-induced expression, the release of adhesion molecules, cytokines and chemokines, and the adenosine diphosphate-induced expression of platelet P-selectin. Andrographolide exhibits an anti-inflammatory effect by downregulating the p38 mitogen activated protein kinase, signal transducer and activator of transcription 3 and NF-κB pathways (47,48). The present study assessed whether tanshinone IIA and andrographolide exhibited the potential anti-inflammatory effects of atherosclerosis in the established experimental system.…”

Section: Discussionmentioning

confidence: 99%

Establishment of an interleukin-1β-induced inflammation-activated endothelial cell-smooth muscle cell-mononuclear cell co-culture model and evaluation of the anti-inflammatory effects of tanshinone IIA on atherosclerosis

Guo

Chen

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Increasing evidence supports the hypothesis that inflammatory reactions serves an important function in the formation, progression and plaque rupture of atherosclerosis. Interleukin (IL)-1 primarily induces inflammation and is closely associated with the inflammatory environment and the formation of atherosclerosis. The present study aimed to establish an in vitro model for the evaluation of drug efficacy in the intervention of atherosclerosis from the inflammatory perspective, and to observe the anti-inflammatory effects of tanshinone IIA and andrographolide on atherosclerosis. The IL-1β-induced inflammation-activated endothelial cell (EC)-smooth muscle cell (SMC)-mononuclear cell (MC) co-culture model was established, based on the changes in a series of atherosclerosis-associated inflammatory markers secreted by ECs and SMCs. The expression of connexin in ECs, adhesion of MCs and changes in inflammatory signalling molecules were selected as evaluation indices for the inflammatory microenvironment of atherosclerosis. The use of this model revealed that tanshinone IIA exhibited significant efficacy against atherosclerosis and its inflammatory reactions. Inflammatory reactions were regarded as the primary mechanism underlying atherosclerosis. The established model simulated a series of relevant changes in the arterial wall under the inflammatory cytokines with oxidized low-density lipoprotein during the atherosclerotic process. The present study presented a reliable method for the identification of drugs with potential anti-inflammatory activity in atherosclerosis, for investigating the mechanisms of action, considering the improvement of the inflammatory state and the increase in plaque stability observed.

show abstract

“…Genetic deletion or pharmacological inhibition of STAT3 would be useful to address this question. It should be noted that andrographolide could also exert various biological effects through suppression of the STAT3 pathway . Water‐soluble andrographolide sulfonate shows antisepsis effects in mice through downregulating p38 MAPK, STAT3, and NF‐κB pathways .…”

Section: Discussionmentioning

confidence: 99%

Andrographolide Protects against Cigarette Smoke‐Induced Lung Inflammation through Activation of Heme Oxygenase‐1

Yang

Zhang

Song

et al. 2013

J Biochem & Molecular Tox

View full text Add to dashboard Cite

This study was conducted to check whether andrographolide, a bioactive molecule isolated from Andrographis paniculata, could protect against cigarette smoke (CS)-induced lung injury through activation of heme oxygenase-1 (HO-1). Pretreatment with andrographolide (1 mg/kg body weight) markedly attenuated lung inflammation in CS-exposed mice, coupled with reduced numbers of total cells, neutrophils, and macrophages in bronchial alveolar lavage fluid (BALF) and decreased production of cytokine/chemokine into BALF. Furthermore, andrographolide pretreatment increased the expression and activation of HO-1 in the lung of CS-exposed animals. Notably, these histological and biochemical changes induced by andrographolide were blocked by prior administration of zinc protoporphyrin IX (ZnPP; 20 mg/kg body weight), a potent heme oxygenase inhibitor. Moreover, andrographolide-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) was attenuated by ZnPP treatment in CS-exposed animals. Our data collectively demonstrate that andrographolide confers protection against CS-induced lung inflammation, partially through activation of HO-1 and STAT3.

show abstract

Water-soluble andrographolide sulfonate exerts anti-sepsis action in mice through down-regulating p38 MAPK, STAT3 and NF-κB pathways

Cited by 62 publications

References 34 publications

Cannabinoid Receptor 2 Protects against Acute Experimental Sepsis in Mice

Cannabinoid Receptor 2 Protects against Acute Experimental Sepsis in Mice

Establishment of an interleukin-1β-induced inflammation-activated endothelial cell-smooth muscle cell-mononuclear cell co-culture model and evaluation of the anti-inflammatory effects of tanshinone IIA on atherosclerosis

Andrographolide Protects against Cigarette Smoke‐Induced Lung Inflammation through Activation of Heme Oxygenase‐1

Contact Info

Product

Resources

About