scholarly journals Neutral Polysaccharide from the Leaves of Pseuderanthemum carruthersii: Presence of 3-O-Methyl Galactose and Anti-Inflammatory Activity in LPS-Stimulated RAW 264.7 Cells

Polymers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1219 ◽  
Author(s):  
Vo Hoai Bac ◽  
Berit Smestad Paulsen ◽  
Le Van Truong ◽  
Andreas Koschella ◽  
Tat Cuong Trinh ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Water Extract ◽  
Mapk Signaling ◽  
Raw 264.7 Cells ◽  
Oxygen Species ◽  
Inflammatory Cytokine Production ◽  
Mouse Macrophages ◽  
Chemotaxonomic Marker

Pseuderanthemum carruthersii (Seem.) Guillaumin is a native tree in Vietnam. The water extract of the leaves from this tree gives a highly viscous product that has been used to heal wounds and treat inflammations. Our previous studies showed that the leaves of P. carruthersii have a high content of polysaccharides. In this study, the structure and influence of the neutral polysaccharide from Pseuderanthemum carruthersii (PCA1) on lipopolysaccharide (LPS)-stimulated RAW264.7 cells were investigated. The PCA1 isolated from P. carruthersii is a galactan-type polysaccharide, containing galactose (77.0%), 3-O-methyl galactose (20.0%), and arabinose (3.0%). Linkage analysis of PCA1 showed that both the 3-O-methyl galactose and galactose were 1,4-linked. The presence of 3-O-methyl galactose units as part of the polysaccharide is important and can be used as a chemotaxonomic marker. The molecular weight of the PCA1 was 170 kDa. A PCA1 concentration of 30–40 μg/mL strongly inhibited TNFα, IL-1β, and IL-6 inflammatory cytokine production, and reactive oxygen species (ROS) release. PCA1 had inhibitory activities on pro-inflammatory cytokine and ROS release in LPS-stimulated mouse macrophages in vitro through MAPK signaling.

scholarly journals Effective fraction of Bletilla striata reduces the inflammatory cytokine production induced by water and organic extracts of airborne fine particulate matter (PM2.5) in vitro

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yu-Yao Zu ◽  
Quan-Fang Liu ◽  
Shu-Xin Tian ◽  
Li-Xia Jin ◽  
Fu-Sheng Jiang ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Dose Range ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Bletilla Striata ◽  
Inflammatory Cytokine Production ◽  
Effective Fraction ◽  
Organic Extracts

Abstract Background Bletilla striata is a traditional Chinese medicine used to treat hemorrhage, scald, gastric ulcer, pulmonary diseases and inflammations. In this study, we investigated bioactivity of the effective fraction of B. striata (EFB) in reducing the inflammatory cytokine production induced by water or organic extracts of PM2.5. Methods PM2.5 extracts were collected and analyzed by chromatographic system and inductively coupled plasma mass spectrometer. Cell viability was measured using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay, and cell supernatant was analyzed by flow cytometry, ELISA, and qRT-PCR in cultured mouse macrophage cell line RAW264.7 treated with EFB and PM2.5 extracts. Expressions of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathway were measured by Western blot. Results PM2.5 composition is complex and the toxicity of PM2.5 extracts were not noticeable. The treatment of EFB at a wide dose-range of 0–40 μg/mL did not cause significant change of RAW264.7 cell proliferation. EFB pretreatment decreased the inflammatory cytokines in the macrophage. Further analysis showed that EFB significantly attenuated PM2.5-induced proinflammatory protein expression and downregulated the levels of phosphorylated NF-κBp65, inhibitor of kappa B (IκB)-α, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38. Conclusions Our study demonstrated the potential effectiveness of B. striata extracts for treating PM2.5-triggered pulmonary inflammation.

scholarly journals Antifungal antibiotics modulate the pro-inflammatory cytokine production and phagocytic activity of human monocytes in an in vitro sepsis model

Life Sciences ◽  
2015 ◽  
Vol 141 ◽  
pp. 128-136 ◽  
Author(s):  
Stefan Muenster ◽  
Christian Bode ◽  
Britta Diedrich ◽  
Sebastian Jahnert ◽  
Christina Weisheit ◽  
...  
Keyword(s):  
Phagocytic Activity ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Human Monocytes ◽  
Inflammatory Cytokine Production ◽  
Sepsis Model ◽  
Antifungal Antibiotics

In vivo and in vitro effects of fluoroquinolones on lipopolysaccharide-induced pro-inflammatory cytokine production

2009 ◽  
Vol 15 (3) ◽  
pp. 168-173 ◽  
Author(s):  
Hiromi Ogino ◽  
Miho Fujii ◽  
Mariko Ono ◽  
Kayoko Maezawa ◽  
Junko Kizu ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production ◽  
In Vitro Effects

scholarly journals 839 Spirulina stimulates inflammatory cytokine production in dermatomyositis in vitro

2020 ◽  
Vol 140 (7) ◽  
pp. S109
Author(s):  
C. Bax ◽  
Y. Li ◽  
A. Ravishankar ◽  
S. Maddukuri ◽  
J. Patel ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

scholarly journals Poxvirus-encoded TNF receptor homolog dampens inflammation and protects from uncontrolled lung pathology during respiratory infection

2020 ◽  
Vol 117 (43) ◽  
pp. 26885-26894
Author(s):  
Zahrah Al Rumaih ◽  
Ma. Junaliah Tuazon Kels ◽  
Esther Ng ◽  
Pratikshya Pandey ◽  
Sergio M. Pontejo ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Tumor Necrosis Factor Receptor ◽  
Binding Domain ◽  
Lung Pathology ◽  
Protective Effects ◽  
Inflammatory Cytokine Production ◽  
Reverse Signaling ◽  
Ifn Γ

Ectromelia virus (ECTV) causes mousepox, a surrogate mouse model for smallpox caused by variola virus in humans. Both orthopoxviruses encode tumor necrosis factor receptor (TNFR) homologs or viral TNFR (vTNFR). These homologs are termed cytokine response modifier (Crm) proteins, containing a TNF-binding domain and a chemokine-binding domain called smallpox virus-encoded chemokine receptor (SECRET) domain. ECTV encodes one vTNFR known as CrmD. Infection of ECTV-resistant C57BL/6 mice with a CrmD deletion mutant virus resulted in uniform mortality due to excessive TNF secretion and dysregulated inflammatory cytokine production. CrmD dampened pathology, leukocyte recruitment, and inflammatory cytokine production in lungs including TNF, IL-6, IL-10, and IFN-γ. Blockade of TNF, IL-6, or IL-10R function with monoclonal antibodies reduced lung pathology and provided 60 to 100% protection from otherwise lethal infection. IFN-γ caused lung pathology only when both the TNF-binding and SECRET domains were absent. Presence of the SECRET domain alone induced significantly higher levels of IL-1β, IL-6, and IL-10, likely overcoming any protective effects that might have been afforded by anti–IFN-γ treatment. The use of TNF-deficient mice and those that express only membrane-associated but not secreted TNF revealed that CrmD is critically dependent on host TNF for its function. In vitro, recombinant Crm proteins from different orthopoxviruses bound to membrane-associated TNF and dampened inflammatory gene expression through reverse signaling. CrmD does not affect virus replication; however, it provides the host advantage by enabling survival. Host survival would facilitate virus spread, which would also provide an advantage to the virus.

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