scholarly journals Engelharquinone suppresses lipopolysaccharide-induced inflammation and proliferation of human liver cancer SMCC7721 cells via inhibition of NF-κB and MAPK signaling pathway

2020 ◽  
Vol 19 (4) ◽  
pp. 699-706
Author(s):  
Shan Li ◽  
Yan Zhang ◽  
Aishe Gao ◽  
Yue Zhang ◽  
Jiong Zhang
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Human Liver ◽  
Mapk Signaling ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Human Liver Cancer ◽  
Mapk Signaling Pathways

Purpose: To investigate the anti-tumor effect of engelharquinone (Eng) on human liver cancer SMCC7721 cells.Methods: GFP-labeled SMCC7721 cells were used to establish a tumor-bearing mice model used for determination of the effect of different  concentrations of Eng on tumor growth. The effect of Eng on SMCC7721 cell viability was determined with MTT assay and cell cycle analysis. The anti-inflammatory effect of Eng on lipopolysaccharide (LPS)-treated SMCC7721 cells were determined through assay of pro-inflammatory cytokines. Besides, the effect of Eng on the expressions of mitogen-activated protein kinase (MAPK), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) was determined.Results: Cell proliferation was suppressed by different concentrations of Eng in LPS-treated SMCC7721 cells. Treatment of nude mice with Eng at high and low doses resulted in significant suppression of tumor growth and marked increases in percentage survival. Treatment of SMCC7721 cells with LPS upregulated the expressions of NF-κB, p65 and MAPK. However, pre-treatment of the cells with Eng suppressed the LPS-induced upregulation of the NF-κB, p65 and MAPK signaling pathways, and further downregulated the production of inflammatory cytokines in SMCC7721 cells.Conclusion: These results indicate that Eng inhibits LPS-induced inflammation and proliferation of human liver cancer SMCC7721 cells via a mechanism involving regulation of NF-κB and MAPK signaling pathways. Thus, Eng has potentials for the clinical management of inflammatory diseases and liver cancer. Keywords: Inflammation, Engelharquinone, Lipopolysaccharide, SMCC7721 cells, Toll-like receptor 4

scholarly journals Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

2016 ◽  
Vol 12 (2) ◽  
pp. 995-1000 ◽  
Author(s):  
Le-Wen Shao ◽  
Li-Hua Huang ◽  
Sheng Yan ◽  
Jian-Di Jin ◽  
Shao-Yan Ren
Keyword(s):  
Liver Cancer ◽  
Signaling Pathways ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Human Liver Cancer

Berberine inhibits lipopolysaccharide-induced expression of inflammatory cytokines by suppressing TLR4-mediated NF-ĸB and MAPK signaling pathways in rumen epithelial cells of Holstein calves

2019 ◽  
Vol 86 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Chenxu Zhao ◽  
Yazhou Wang ◽  
Xue Yuan ◽  
Guoquan Sun ◽  
Bingyu Shen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Drug ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways ◽  
Rumen Epithelial Cells

AbstractSubacute ruminal acidosis (SARA) can increase the level of inflammation and induce rumenitis in dairy cows. Berberine (BBR) is the major active component of Rhizoma Coptidis, which is a type of Chinese anti-inflammatory drug for gastrointestinal diseases. The purpose of this study was to investigate the anti-inflammatory effects of BBR on lipopolysaccharide (LPS)-stimulated rumen epithelial cells (REC) and the underlying molecular mechanisms. REC were cultured and stimulated with LPS in the presence or absence of different concentrations of BBR. The results showed that cell viability was not affected by BBR. Moreover, BBR markedly decreased the concentrations and mRNA expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the LPS-treated REC in a dose-dependent manner. Importantly, Western blotting analysis showed that BBR significantly suppressed the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and the phosphorylation of nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) in LPS-treated REC. Furthermore, the results of immunocytofluorescence showed that BBR significantly inhibited the nuclear translocation of NF-κB p65 induced by LPS treatment. In conclusion, the protective effects of BBR on LPS-induced inflammatory responses in REC may be due to its ability to suppress the TLR4-mediated NF-κB and MAPK signaling pathways. These findings suggest that BBR can be used as an anti-inflammatory drug to treat inflammation induced by SARA.

scholarly journals Andrographolide Derivative AL-1 Ameliorates Dextran Sodium Sulfate-Induced Murine Colitis by Inhibiting NF-κB and MAPK Signaling Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Mei Jing ◽  
Yuqiang Wang ◽  
Lipeng Xu
Keyword(s):  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Sodium Sulfate ◽  
Mapk Signaling ◽  
Dextran Sodium Sulfate ◽  
Myeloperoxidase Activity ◽  
Altered Expression ◽  
Murine Colitis ◽  
Mapk Signaling Pathways

Trinitrobenzenesulfonic acid (TNBS) and dextran sodium sulfate (DSS) are commonly used to induce experimental murine ulcerative colitis (UC). Our recent study has demonstrated that a novel andrographolide derivative, AL-1, ameliorated TNBS-induced colitis in mice. However, the effect of AL-1 on DSS-induced murine colitis and the underlying mechanisms are yet unknown. In the present study, we aimed to investigate the therapeutic potential of AL-1 against DSS-induced UC in mice and to define its mechanisms of action. Oral administration of AL-1 attenuated body weight loss, reduced colon length shortening, lowered the disease activity index score, and alleviated colon histological damage. AL-1 significantly inhibited myeloperoxidase activity and suppressed immune inflammatory responses in colonic tissues. Moreover, AL-1 reversed DSS-altered expression of inflammatory cytokines in DSS-induced colitis mice. Importantly, the efficacy of 45 mg/kg of AL-1 was higher than that of 100 mg/kg of the positive control drugs 5-aminosalicylic acid and mesalazine. AL-1 decreased lipopolysaccharide-induced generation of reactive oxygen species and nitric oxide in cultured macrophages in vitro; it also reversed the altered expression of inflammatory cytokines. In both in vivo and in vitro studies, Western blot analysis revealed that AL-1 reduced the expression of phosphorylated NF-κB p65 and IκBα, downregulated the expression of iNOS and COX-2, and attenuated the expression of phosphorylated p38 mitogen-activated protein kinase (MAPK), ERK, and JNK. In conclusion, AL-1 alleviated DSS-induced murine colitis by inhibiting activation of the NF-κB and MAPK signaling pathways. Our data suggest that AL-1 could be a potential new treatment for UC.

scholarly journals Sedanolide induces autophagy through the PI3K, p53 and NF-κB signaling pathways in human liver cancer cells

2015 ◽  
Vol 47 (6) ◽  
pp. 2240-2246 ◽  
Author(s):  
SHU-LING HSIEH ◽  
CHI-TSAI CHEN ◽  
JYH-JYE WANG ◽  
YU-HAO KUO ◽  
CHIEN-CHUN LI ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Human Liver ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

scholarly journals Effects of Adipose-Derived Biogenic Nanoparticle-Associated microRNA-451a on Toll-like Receptor 4-Induced Cytokines

Pharmaceutics ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 16
Author(s):  
Xinghua Wang ◽  
Anthony Pham ◽  
Lu Kang ◽  
Sierra A. Walker ◽  
Irina Davidovich ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Signaling Pathways ◽  
Extracellular Vesicles ◽  
Inflammatory Cytokines ◽  
Stromal Cells ◽  
Toll Like Receptor ◽  
Immunomodulatory Effects ◽  
Toll Like Receptor 4 ◽  
Biogenic Nanoparticles ◽  
Pro Inflammatory Cytokines

Extracellular vesicles (EVs) are cell-released nanoparticles that transfer biomolecular content between cells. Among EV-associated biomolecules, microRNAs (miRNAs/miRs) represent one of the most important modulators of signaling pathways in recipient cells. Previous studies have shown that EVs from adipose-derived mesenchymal stromal cells (MSCs) and adipose tissue modulate inflammatory pathways in macrophages. In this study, the effects of miRNAs that are abundant in adipose tissue EVs and other biogenic nanoparticles (BiNPs) were assessed in terms of altering Toll-like receptor 4 (TLR4)-induced cytokines. TLR-4 signaling in macrophages is often triggered by pathogen or damage-induced inflammation and is associated with several diseases. This study demonstrates that miR-451a, which is abundant in adipose tissue BiNPs, suppresses pro-inflammatory cytokines and increases anti-inflammatory cytokines associated with the TLR4 pathway. Therefore, miR-451a may be partially responsible for immunomodulatory effects of adipose tissue-derived BiNPs.

scholarly journals Thymoquinone inhibits angiogenesis and prostate tumor growth by suppressing MAPK signaling pathways

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tingfang Yi ◽  
SungGook Cho ◽  
Zhengfang Yi ◽  
Weijia Luo ◽  
Ying Wang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Prostate Tumor ◽  
Mapk Signaling Pathways
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