Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells

Ji, Guangquan; Chen, Renqiong; Zheng, Jianxian

doi:10.3109/08923973.2014.968256

Cited by 41 publications

(33 citation statements)

References 35 publications

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“…1F). Furthermore, LPS-induced UDP release could be rescued obviously by AOI (a selective inhibitor to TLR4) (24), suggesting the important role of TLR signaling in UDP release (Fig. 1G).…”

Section: Udp Is Released During Bacterial Infectionmentioning

confidence: 92%

TLR-Activated Gap Junction Channels Protect Mice against Bacterial Infection through Extracellular UDP Release

Qin

Zhang

et al. 2016

The Journal of Immunology

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Extracellular UDP (eUDP), released as a danger signal by stressed or apoptotic cells, plays an important role in a series of physiological processes. Although the mechanism of eUDP release in apoptotic cells has been well defined, how the eUDP is released in innate immune responses remains unknown. In this study, we demonstrated that UDP was released in both Escherichia coli–infected mice and LPS- or Pam3CSK4-treated macrophages. Also, LPS-induced UDP release could be significantly blocked by selective TLR4 inhibitor Atractylenolide I and selective gap junction inhibitors carbenoxolone and flufenamic acid (FFA), suggesting the key role of TLR signaling and gap junction channels in this process. Meanwhile, eUDP protected mice from peritonitis by reducing invaded bacteria that could be rescued by MRS2578 (selective P2Y6 receptor inhibitor) and FFA. Then, connexin 43, as one of the gap junction proteins, was found to be clearly increased by LPS in a dose- and time-dependent manner. Furthermore, if we blocked LPS-induced ERK signaling by U0126, the expression of connexin 43 and UDP release was also inhibited dramatically. In addition, UDP-induced MCP-1 secretion was significantly reduced by MRS2578, FFA, and P2Y6 mutation. Accordingly, pretreating mice with U0126 and Gap26 increased invaded bacteria and aggravated mice death. Taken together, our study reveals an internal relationship between danger signals and TLR signaling in innate immune responses, which suggests a potential therapeutic significance of gap junction channel–mediated UDP release in infectious diseases.

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“…1F). Furthermore, LPS-induced UDP release could be rescued obviously by AOI (a selective inhibitor to TLR4) (24), suggesting the important role of TLR signaling in UDP release (Fig. 1G).…”

Section: Udp Is Released During Bacterial Infectionmentioning

confidence: 92%

TLR-Activated Gap Junction Channels Protect Mice against Bacterial Infection through Extracellular UDP Release

Qin

Zhang

et al. 2016

The Journal of Immunology

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“…In order to verify the effect of Lactobacillus on Wnt/β‐catenin signal pathway, budding organoid were also pretreated with Lactobacillus combined with or without Toll‐like receptor 2 inhibitor CU‐CUPT22 (0.02%, Selleck, USA) for 12 h and then the intestinal organoids were infected by S. typhimurium with or without Toll‐like receptor 4 inhibitor atractylenolide I (1%, Selleck, USA) for 1 h …”

Section: Methodsmentioning

confidence: 99%

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

Xiao

Xie

et al. 2020

Molecular Nutrition Food Res

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Scope The influence of the intestinal microbiota, such as Lactobacillus, on the intestinal mucosa, particularly intestinal stem cells, remains incompletely understood. In this study, mice and intestinal organoids are used to explore the regulatory effect of Lactobacillus on the proliferation and differentiation of intestinal epithelial cells. Methods and results This study demonstrates that S. typhimurium causes intestinal epithelial damage and affected growth of intestinal organoids. S. typhimurium also colonizes the intestine and then causes pathological changes to the intestinal epithelium, intestinal inflammation, and even death. However, L. acidophilus alleviates damage to intestinal organoids, increases the survival ratio of mice infected with S. typhimurium, and reduces tumor necrosis factor‐α (TNF‐α) secretion. Moreover, L. acidophilus affects the differentiation of epithelial cells through inhibition of the excessive expansion of goblet cells and Paneth cells induced by S. typhimurium to avoid over‐exhaustion. Finally, it is also demonstrated that L. acidophilus ameliorates overactivation of Wnt/β‐catenin pathway by Salmonella, depending on the contact with toll‐like receptor 2 (TLR2), to affect the proliferation of the intestinal epithelium. Conclusions This study demonstrates that L. acidophilus protects the intestinal mucosa against S. typhimurium infection through not only the inhibition of pathogen invasion but also determination of the fate of the intestinal epithelium.

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“…and exerts a wide range of pharmacological activities, including anti-inflammatory (11,12), anti-tumor (13,14) and anti-angiogenic effects (15). A previous study has implied a potential anti-depressive activity of AT-I (16).…”

Section: Introductionmentioning

confidence: 99%

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Gao

Zhu

et al. 2017

Exp Ther Med

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Abstract. Atractylenolide I (AT-I), a major component of the rhizoma of Atractylodes macrocephala Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.

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Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells

Cited by 41 publications

References 35 publications

TLR-Activated Gap Junction Channels Protect Mice against Bacterial Infection through Extracellular UDP Release

TLR-Activated Gap Junction Channels Protect Mice against Bacterial Infection through Extracellular UDP Release

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

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