Abstract
Sakuranetin is flavonoid phytoalexin that serves as a plant antibiotic and exists in Prunus and several other plant species. Recently, we identified the anti-inflammatory effect of Prunus yedoensis and found that there were few studies on the potential anti-inflammatory activity of sakuranetin, one of the main constituents of Prunus yedoensis. Here, we isolated peritoneal macrophages from thioglycollate-injected mice and examined whether sakuranetin affected the response of the macrophages in response to lipopolysaccharide (LPS) plus interferon- (IFN-) γ or LPS only. Sakuranetin suppressed the synthesis of iNOS and COX2 in LPS/IFN-γ stimulated cells and the secretion of TNF-α, IL-6, and IL-12 in LPS stimulated cells. The surface expression of the costimulatory molecules, CD86 and CD40, was also decreased. Among the LPS-induced signaling molecules, STAT1, JNK, and p38 phosphorylation was attenuated. These findings are evidence that sakuranetin acts as anti-inflammatory flavonoid and further study is required to evaluate its in vivo efficacy.
Highlights
Inflammatory responses are protective against further tissue damage and help to repair wounds
Macrophages recognize the presence of the causative agent through pattern recognition receptors such as toll-like receptor (TLR) and activate the NF-κB pathway and mitogenactivated protein kinases (MAPK) pathway, terminating in the expression of inflammatory enzymes such as inducible nitric oxide synthases and cyclooxygenase- (COX-) 2 and inflammatory cytokines such as tumor necrosis factor(TNF-) α, interleukin- (IL-) 6, and IL-12 [3]
A culture of peritoneal macrophages incubated with 200 μM for 24 h resulted in no effect on cell viability, but cells incubated with 400 μM sakuranetin showed a rapid decrease in number (Figure 1)
Summary
Inflammatory responses are protective against further tissue damage and help to repair wounds. The reasons for the chronicity of inflammation include microbes that evade the immune system, accumulating metabolic or cellular byproducts, and autoimmune diseases generated by unknown causes. Depending on the time required to initially respond, the site of first contact with the antigen, and the ability to acquire memory, the immune system is divided into innate and adaptive systems. Cells that belong to the innate immune system confront the antigens and respond to them immediately but do not acquire memory. Adaptive immune cells make first contact with antigens in secondary lymphoid tissue such as lymph nodes, which explains why they take time to respond, and acquire memory, letting the cells mount a faster response to the exposure of the antigen. The above molecules are targets of anti-inflammatory agents for the control of chronic inflammation
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