Wu CH, Chen TL, Chen TG, Ho WP, Chen RM |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=55 ------>confirm_bywho=soulchin ------>insert_bywho=chwu ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=545 ------>medlineContent= ------>unit=E0110 ------>insert_date=20030507 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=7 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=The Journal of Trauma ------>paper_name=Nitric oxide modulates pro-and anti-inflammatory cytokines in lipopolysaccharide-activated macrophages ------>confirm_date=20040507 ------>tch_id=071004 ------>pmid=14501900 ------>page1=540 ------>fullAbstract=BACKGROUND: Sepsis is a serious and life-threatening syndrome that occurs in intensive care unit patients. Lipopolysaccharide (LPS) has been implicated as one of major causes of sepsis. Nitric oxide (NO) and cytokines are involved in sepsis-induced inflammatory responses. This study is aimed at evaluating the effects of NO on the modulation of pro- and anti-inflammatory cytokines in LPS-activated macrophages and its possible mechanism. METHODS: N-Monomethyl arginine (NMMA), an inhibitor of NO synthase, was used in this study to suppress NO production. Mouse macrophage-like Raw 264.7 cells were exposed to LPS, NMMA, or a combination of NMMA and LPS. Cell viability was determined by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-di-phenyltetrazolium bromide assay. The amounts of nitrite, an oxidative product of NO, in the culture medium were quantified according to the Griess reaction method. Enzyme-linked immunosorbent assay and reverse-transcriptase polymerase chain reaction were carried out to determine the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-10 in macrophages. RESULTS: Exposure of macrophages to LPS, NMMA, and a combination of NMMA and LPS for 24 hours did not affect cell viability. LPS significantly increased the amounts of nitrite in macrophages (p < 0.01). Treatment with NMMA decreased LPS-enhanced nitrite (p < 0.01) in a concentration-dependent manner. Analyses of enzyme-linked immunosorbent assays and reverse-transcriptase polymerase chain reaction revealed that LPS significantly induced TNF-alpha, IL-1 beta, and IL-10 proteins and mRNA (p < 0.01). A combined treatment with NMMA and LPS significantly blocked LPS-induced TNF-alpha and IL-1 beta (p < 0.01), but synergistically enhanced LPS-induced IL-10 (p < 0.05) protein and RNA. CONCLUSION: This study has shown that NO suppression can inhibit LPS-induced TNF-alpha and IL-1 beta but enhance IL-10, and the modulation occurs at a pretranslational level. ------>tmu_sno=None ------>sno=7221 ------>authors2= ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Wu CH, Chen TL, Chen TG, Ho WP, Chen RM ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Nitric oxide modulates pro- and anti-inflammatory cytokines in lipopolysaccharide-activated macrophages. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho= ------>publish_year=2003 ------>submit_flag= ------>publish_month=None |