Abstract
BackgroundCudrania tricuspidata extract is an important traditional herbal remedy for tumors, inflammation, gastritis, and liver damage and is predominantly used in Korea, China, and Japan. However, the anti-inflammatory effects of the extract have not yet been conclusively proved.MethodsIn this study, we investigated the effects of the CHCl3 fraction (CTC) of a methanol extract of C. tricuspidata on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 macrophage cells and mouse peritoneal macrophages, and the levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in RAW 264.7 macrophage cells.ResultsWe observed that the protein expression levels of inducible NO synthase and COX-2 enzymes were markedly inhibited by CTC in a concentration-dependent manner. In addition, CTC reduced the production of TNF-α, IL-1β, and IL-6 in the LPS-stimulated RAW 264.7 macrophage cells.ConclusionsOur results show that the C. tricuspidata extract could modulate macrophage-mediated inflammatory functions such as the overproduction of cytokines, NO, and PGE2. The CTC was found to be the active fraction in this context.
Highlights
Cudrania tricuspidata extract is an important traditional herbal remedy for tumors, inflammation, gastritis, and liver damage and is predominantly used in Korea, China, and Japan
We show that CTC reduces the production of nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-α (TNF-α) in RAW 264.7 cells and mouse macrophage cells when these cells are treated with recombinant LPS
Effects of CTC on LPS-induced NO and PGE2 production To investigate the anti-inflammatory properties of CTC, we used RAW 264.7 cells, which produce NO and PGE2 when stimulated by LPS
Summary
Cudrania tricuspidata extract is an important traditional herbal remedy for tumors, inflammation, gastritis, and liver damage and is predominantly used in Korea, China, and Japan. Like LPS, activate cytokine networks by inducing many proinflammatory genes. These inductions are mediated via the activation of inducible transcription factors [7]. Large amounts of the pro-inflammatory mediators NO and prostaglandin E2 (PGE2) are generated by the inducible isoforms of NO synthase (NOS) and cyclooxygenase-2 (COX-2) [8]. NO is synthesized by 3 isoforms of NOS, namely, neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS). NNOS and eNOS are constitutively expressed, iNOS is expressed in response to interferon-γ (IFN-γ), LPS, and various pro-inflammatory cytokines [9,10]. Inhibiting the production of NO and PGE2 is an important therapeutic target in the development of anti-inflammatory agents
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