Corylin inhibits LPS-induced inflammatory response and attenuates the activation of NLRP3 inflammasome in microglia

Huang, Ming-Yii; Tu, Chia-En; Wang, Shu-Chi; Hung, Yung-Li; Su, Chin-Chuan; Fang, Shih-Hua; Chen, Chi-Shuo; Liu, Po-Len; Cheng, Wei‐Chung; Huang, Yuwei; Li, Chia-Yang

doi:10.1186/s12906-018-2287-5

Cited by 58 publications

(37 citation statements)

References 37 publications

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“…The NLRP3 inflammasome plays a critical role in the LPS-induced inflammation model. 32 Consistent with that study, the expression of NLRP3, ASC, and the levels of activated caspase-1 in this study were significantly upregulated in LPS-treated groups compared with the control groups ( Figure 2A – D #P<0.01). In addition, the expression of Pro-IL-1β ( Figure 2E ), IL-1β ( Figure 2F ) and the production of IL-1β ( Figure 2G ) by ELISA were increased in the LPS-treated group compared with control groups (#P<0.01).…”

Section: Resultssupporting

confidence: 90%

<p>Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inﬂammasome Activation</p>

Chen

Liu

Zhu

et al. 2020

CMAR

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Background Inflammation is considered as one of the hallmarks of cancer development and progression. Ursolic acid (UA) showed strong effects as an anti-inflammatory and antioxidant. However, the anti-cancer effects of ursolic acid require further study. Methods This study aimed to investigate the role of ursolic acid in a lipopolysaccharide (LPS)-treated gastric tumour mouse model and in a human gastric carcinoma cell line (BGC-823 cells). This study also aimed to confirm whether ursolic acid can protect against proliferation and the inflammatory response induced by LPS, by inhibiting the activation of the NLRP3 inflammasome via the NF-κB pathway. Results The present study demonstrated that ursolic acid significantly attenuated LPS-treated proliferation in a gastric tumour mouse model and the human gastric carcinoma BGC-823 cell line, reduced the expression of the NLRP3 inflammasome and suppressed the release of pro-inflammatory cytokines. In addition, ursolic acid inhibited the LPS-induced activation of NF-κB. Furthermore, the NF-κB pathway regulated the activation of the NLRP3 inﬂammasome. Conclusion In conclusion, these results demonstrated that ursolic acid could suppress proliferation and the inflammatory response in an LPS-induced mouse gastric tumour model and human BGC-823 cells by inhibiting the activation of the NLRP3 inﬂammasome via the NF-κB pathway. This indicates that ursolic acid can be a potential therapeutic agent for the treatment of gastric cancer.

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Section: Resultssupporting

confidence: 90%

<p>Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inﬂammasome Activation</p>

Chen

Liu

Zhu

et al. 2020

CMAR

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“…Similar results were found when BV2 were challenged with LPS alone (in absence of ATP treatment) (Supplementary Figures S3 , S4 ), thus supporting that TLR4 stimulation alone may drive inflammasome priming and activation in BV2 cells without the need for a secondary signal. This distinctive one-step pathway of inflammasome activation is typically seen in monocytes and have been recently seen in recent studies using BV2 cells ( Carta et al, 2011 ; Huang M.Y. et al, 2018 ; Yang et al, 2018 ).…”

Section: Resultssupporting

confidence: 52%

Divergent Effects of Metformin on an Inflammatory Model of Parkinson’s Disease

Tayara

Espinosa-Oliva

García-Domínguez

et al. 2018

Front. Cell. Neurosci.

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The oral antidiabetic drug metformin is known to exhibit anti-inflammatory properties through activation of AMP kinase, thus protecting various brain tissues as cortical neurons, for example. However, the effect of metformin on the substantia nigra (SN), the main structure affected in Parkinson’s disease (PD), has not yet been studied in depth. Inflammation is a key feature of PD and it may play a central role in the neurodegeneration that takes place in this disorder. The aim of this work was to determine the effect of metformin on the microglial activation of the SN of rats using the animal model of PD based on the injection of the pro-inflammogen lipopolysaccharide (LPS). In vivo and in vitro experiments were conducted to study the activation of microglia at both the cellular and molecular levels. Our results indicate that metformin overall inhibits microglia activation measured by OX-6 (MHCII marker), IKKβ (pro-inflammatory marker) and arginase (anti-inflammatory marker) immunoreactivity. In addition, qPCR experiments reveal that metformin treatment minimizes the expression levels of several pro- and anti-inflammatory cytokines. Mechanistically, the drug decreases the phosphorylated forms of mitogen-activated protein kinases (MAPKs) as well as ROS generation through the inhibition of the NADPH oxidase enzyme. However, metformin treatment fails to protect the dopaminergic neurons of SN in response to intranigral LPS. These findings suggest that metformin could have both beneficial and harmful pharmacological effects and raise the question about the potential use of metformin for the prevention and treatment of PD.

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“…Rat microglia were cultured as previously described (Nakajima et al, 1992; Nakajima and Kohsaka, 1993; Shigemoto-Mogami et al, 2014). To activate microglia, they were incubated with 1 μg/ml LPS for 1 h (LPS-MG), which has already been shown to induce inflammatory reaction in our preliminary experiments and another's report (Huang et al, 2018). Microglia were then washed twice, and transferred to the abluminal side of the BBB model at 5.0 × 10 4 cells/cm 2 .…”

Section: Methodsmentioning

confidence: 99%

Activated Microglia Disrupt the Blood-Brain Barrier and Induce Chemokines and Cytokines in a Rat in vitro Model

Shigemoto-Mogami

Hoshikawa

Sato

2018

Front. Cell. Neurosci.

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Severe neuroinflammation is associated with blood brain barrier (BBB) disruption in CNS diseases. Although microglial activation and the subsequent changes in cytokine/chemokine (C/C) concentrations are thought to be key steps in the development of neuroinflammation, little data are available concerning the interaction of microglia with BBB cells. In this study, we investigated this interaction by adding LPS-activated microglia (LPS-MG) to the abluminal side of a BBB model composed of endothelial cells (EC), pericytes (Peri) and astrocytes (Ast). We then examined the abluminal concentrations of 27 C/Cs and the interactions between the LPS-MG and BBB cells. LPS-MG caused collapse of the BBB, revealed by decreases in the trans-endothelial electrical resistance (TEER) and by changes in the expression levels of tight junction (TJ) proteins. Under these conditions, 19 C/Cs were markedly increased on the abluminal side. Unexpectedly, although LPS-MG alone released 10 of the 19 C/Cs, their concentrations were much lower than those detected on the abluminal side of the BBB model supplemented with LPS-MG. Co-culture of LPS-MG with Ast caused marked increases in 12 of the 19 C/Cs, while co-culture of LPS-MG with EC and Peri resulted in a significant increase in only 1 of the 19 C/Cs (fractalkine). These results suggest that C/C dynamics in this system are not only caused by activated microglia but also are due to the interaction between activated microglia and astrocytes.

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Corylin inhibits LPS-induced inflammatory response and attenuates the activation of NLRP3 inflammasome in microglia

Cited by 58 publications

References 37 publications

<p>Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inﬂammasome Activation</p>

<p>Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inﬂammasome Activation</p>

Divergent Effects of Metformin on an Inflammatory Model of Parkinson’s Disease

Activated Microglia Disrupt the Blood-Brain Barrier and Induce Chemokines and Cytokines in a Rat in vitro Model

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