Objective: To investigate the effects of human umbilical cord mesenchymal stem cells (hUCMSCs) on the polarization of lipopolysaccharide-stimulated RAW264.7 macrophages.
Methods: Lipopolysaccharide-stimulated RAW264.7 macrophages were co-cultured with hUCMSCs in a Transwell system for 4 d, and then labelled with anti-F4/80, anti-CD86, and anti-CD206 antibodies for flow cytometry. The co-cultured supernatants were detected by enzyme-linked immunosorbent assay for prostaglandin E2. The co-cultured RAW264.7 macrophages were also lysed to measure the intracellular level of inducible nitric oxide synthase.
Results: There were significantly more F4/80+CD86+CD206+ RAW264.7 macrophages in the hUCMSCs-treated groups than the control group (P<0.001). The secretion of prostaglandin E2 by lipopolysaccharide-stimulated RAW264.7 macrophages was significantly inhibited in a dose-dependent manner with the addition of hUCMSCs (P<0.001). The expression of iNOS, the intracellular marker of M1 cells, was also significantly inhibited by hUCMSCs (P<0.05).
Conclusion: hUCMSCs significantly polarize the lipopolysaccharide-stimulated RAW264.7 macrophages from a pro-inflammatory M1 subpopulation to an intermediate subpopulation of anti-inflammatory M2 macrophages, which are associated with a gradual decrease of iNOS and PGE levels.
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Chem Biodivers
December 2023
Institute of Chemistry, VAST, 18 Hoang Quoc Viet, Cau Giay, Hanoi, 10000, Vietnam.
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August 2014
Swiss Hepato-Pancreatico-Biliary Center, Department of Surgery, University Hospital Zürich, CH-8091 Zürich, Switzerland. Electronic address:
Background & Aims: Fasting and calorie restriction are associated with a prolonged life span and an increased resistance to stress. The protective effects of fasting have been exploited for the mitigation of ischemic organ injury, yet the underlying mechanisms remain incompletely understood. Here, we investigated whether fasting protects liver against ischemia reperfusion (IR) through energy-preserving or anti-inflammatory mechanisms.
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October 2013
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J Immunol
March 2009
Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Valladolid, Spain.
Macrophages can be activated through TLRs for a variety of innate immune responses. In contrast with the wealth of data existing on TLR-dependent gene expression and resultant cytokine production, very little is known on the mechanisms governing TLR-mediated arachidonic acid (AA) mobilization and subsequent eicosanoid production. We have previously reported the involvement of both cytosolic group IVA phospholipase A(2) (cPLA(2)) and secreted group V phospholipase A(2) (sPLA(2)-V) in regulating the AA mobilization response of macrophages exposed to bacterial LPS, a TLR4 agonist.
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September 1997
First Department of Internal Medicine, Nagoya University School of Medicine, Aichi, Japan.
Murine interferon-gamma (IFN-gamma) stimulates the murine macrophage tumour cell line RAW264-7 to produce nitric oxide (NO). IFN-gamma induces expression of inducible NO synthase (iNOS), manganese superoxide dismutase (Mn-SOD) and copper zinc SOD (CuZn-SOD) in these cells. To investigate the mechanism of induction of SOD expression, we added S-nitroso-N-acetyl penicillamine (SNAP) to RAW264-7 cells.
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