Lipopolysaccharide-Induced Nitric Oxide and Prostaglandin E2 Production Is Inhibited by Tellimagrandin II in Mouse and Human Macrophages
Autor: | Yen-Hsu Chen, Chun-Yu Lin, Yu-Wei Chang, Shih-Han Kao, Wen-Hung Wang, Hsin-Ju Chien, Ling-Chien Hung |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Lipopolysaccharide Science Immunology Inflammation macrophage General Biochemistry Genetics and Molecular Biology Article Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine nitric oxide Tellimagrandin II medicine Viability assay Prostaglandin E2 Cytotoxicity Ecology Evolution Behavior and Systematics biology Chemistry Kinase Paleontology Cell biology Nitric oxide synthase 030104 developmental biology Space and Planetary Science inflammation cyclooxygenase-2 030220 oncology & carcinogenesis Immunologi biology.protein medicine.symptom medicine.drug |
Zdroj: | Life Volume 11 Issue 5 Life, Vol 11, Iss 411, p 411 (2021) |
ISSN: | 2075-1729 |
DOI: | 10.3390/life11050411 |
Popis: | Sepsis develops from a serious microbial infection that causes the immune system to go into overdrive. The major microorganisms that induce sepsis are Gram-negative bacteria with lipopolysaccharide (LPS) in their cell walls. Nitric oxide (NO) and cyclooxygenase-2 (COX-2) are the key factors involved in the LPS-induced pro-inflammatory process. This study aimed to evaluate the effects of polyphenol Tellimagrandin II (TGII) on anti-inflammatory activity and its underlying basic mechanism in murine macrophage cell line RAW 264.7 and human monocyte-derived macrophages. Macrophages with more than 90% cell viability were found in the cytotoxicity assay under 50 μM TGII. Pre- or post-treatment with TGII significantly reduced LPS-induced inducible nitric oxide synthase (NOS2) protein and mRNA expression, reducing LPS-induced COX-2 protein. Downstream of NOS2 and COX-2, NO and prostaglandin E2 (PGE2) were significantly inhibited by TGII. Upstream of NOS2 and COX-2, phospho-p65, c-fos and phospho-c-jun were also reduced after pre-treatment with TGII. Mitogen-activated protein kinases (MAPKs) are also critical to nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) stimulation, and phospho-p38 expression was found to have been blocked by TGII. TGII efficiently reduces LPS-induced NO production and its upstream regulatory factors, suggesting that TGII may be a potential therapeutic agent for sepsis and other inflammatory diseases. |
Databáze: | OpenAIRE |
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