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Effect of Ethanol Extracts of Guava Seeds on Cytokine Secretions Using Mouse Peritoneal Macrophages in Vitro
|關鍵字:||Anti-inflammation;Cytokine;Ethanol extract;Guava seed;抗發炎;細胞激素;乙醇萃取物;芭樂籽||出版社:||臺中巿： 國立中興大學農學院||Project:||農林學報, Volume 62, Issue 2, Page(s) 145-157.||摘要:||
In our preliminary study we found that there are immunomodulatory components in guava seeds, however effective components in guava seeds are difficult to be ingested directly. To obtain effective components and evaluate their possible immunomodulatory functions, guava seeds were extracted with 80% alcohol in this study. The isolated ethanol extracts of guava seeds (EEGS) were subjected to cytotoxic effect assay using mouse peritoneal macrophages to achieve optimal non-cytotoxic concentrations. The adopted optimal concentrations were cultured with mouse peritoneal macrophages in the absence or presence of lipopolysaccharide (LPS) for evaluating the effect of EEGS on cytokine secretions. The results showed that EEGS administered from 4 to 250μg/ml had not apparent cytotoxic effects on peritoneal macrophages, indicating optimal concentrations to the cells. The optimal concentrations were further administered to mouse peritoneal macrophages to assay cytokine secretion profiles. In the absence of LPS, both pro-inflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-6 and an anti-inflammatory cytokine (IL-10) secretion levels significantly (P＜0.05) increased by EEGS dose-dependently. Pro-/anti-inflammatory cytokine secretion ratios by the cells also increased dose-dependently, suggesting that EEGS might activate macrophages and slightly induce spontaneous inflammation. In the presence of LPS, the addition of EEGS significantly decreased pro-/anti-inflammatory cytokine secretion ratio by peritoneal macrophages dose-dependently, suggesting that EEGS might inhibit LPS-induced inflammation in macrophages. In conclusion, we found EEGS possessed immunomodulatory activities. EEGS alone might activate macrophages, but it might inhibit LPS-induced inflammation in macrophages.
|Appears in Collections:||第62卷 第02期|
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