RESUMO
At present, timely and accurate diagnosis and effective treatment of Epstein-Barr Virus (EBV) infection-associated fever remain a difficult challenge. EBV encodes 44 mature microRNAs (miRNAs) that inhibit viral lysis, adjust inflammatory response, regulate cellular apoptosis, promote tumor genesis and metastasis, and regulate tumor cell metabolism. Herein, we have collected the specific expression data of EBV-miRNAs in EBV-related fevers [including infectious mononucleosis (IM), EBV-associated hemophagocytic lymphohistiocytosis (EBV-HLH), chronic active EBV infection (CAEBV), and EBV-related tumors] and proposed the potential value of EBV-miRNAs as biomarkers to assist in the identification, diagnosis, and prognosis of EBV-related fever, as well as therapeutic targets for drug development.
RESUMO
OBJECTIVE@#To investigate the effects of emodin on inflammation and autophagy in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages and reveal its underlying mechanism.@*METHODS@#3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was conducted to find the appropriate dose for emodin. RAW264.7 cells pretreated with different concentrations (0-50 μmol/L) of emodin or vehicle for 2 h prior to exposure to LPS for 16 h. Cell morphology was examined and propidium iodide staining was used to examine cell cycle. Expressions of inflammation-related proteins [nuclear factor-kappaB (NF-κ B) and I-kappaB (I κ B)α] and autophagy-related proteins [light chain (LC)3, P62/sequestosome 1, mammalian target of rapamycin (mTOR), and p-mTOR] were examined using Western blot analysis. Expression of inflammation-related cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were detected by enzyme-linked immunosorbent assay. Autophagy was examined with LC3B fluorescence intensity and aggregation. The effect of emodin on autophagy was conducted with an autophagy inhibitor, 3-methyladenine (3-MA).@*RESULTS@#The expression of NF-κ B in LPS-induced cells was significantly increased (P<0.01) and simultaneously I κ B α decreased compared with the normal cell (P<0.05). The expressions of TNF-α, IL-β, and IL-6 proteins in the LPS-induced RAW264.7 cells were significantly higher than in the normal cell (P<0.05 or P<0.01). LPS increased the percentage of cells in the G@*CONCLUSION@#Emodin could inhibit inflammation of mice RAW264.7 macrophages induced by LPS, possibly through activating autophagy.
