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- Title
Lipopolysaccharide-Induced Nitric Oxide and Prostaglandin E2 Production Is Inhibited by Tellimagrandin II in Mouse and Human Macrophages.
- Authors
Lin, Chun-Yu; Kao, Shih-Han; Hung, Ling-Chien; Chien, Hsin-Ju; Wang, Wen-Hung; Chang, Yu-Wei; Chen, Yen-Hsu; Chadzińska, Magdalena; Lin, Chi-Chien; Lin, Shih-Chao; Carey, Brian
- Abstract
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.
- Subjects
NITRIC-oxide synthases; DINOPROSTONE; NITRIC oxide; MITOGEN-activated protein kinases; PLANT polyphenols; MACROPHAGES; SEPSIS
- Publication
Life (2075-1729), 2021, Vol 11, Issue 5, p411
- ISSN
2075-1729
- Publication type
Article
- DOI
10.3390/life11050411