| Wu GJ |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=3.090 ------>paper_class3=2 ------>paper_class2=1 ------>vol=180 ------>confirm_bywho=wslee ------>insert_bywho=rmchen ------>Jurnal_Rank=15.1 ------>authors4_c= ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=471 ------>medlineContent= ------>unit=E1300 ------>insert_date=20090518 ------>iam=4 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=480 ------>journal_name=Chem-Biol Interact ------>paper_name=Propofol suppresses tumor necrosis factor-? biosynthesis in lipopolysaccharide-stimulated macrophages possibly through downregulation of nuclear factor-kappa B-mediated toll-like receptor 4 gene expression. ------>confirm_date=20091105 ------>tch_id=088008 ------>pmid=19433076 ------>page1=465 ------>fullAbstract=Lipopolysaccharide (LPS), a gram-negative bacterial outer membrane component, can activate macrophages via a toll-like receptor 4-dependent pathway. Our previous study has shown that propofol, an intravenous anesthetic reagent, has anti-inflammatory effects. This study was further aimed to evaluate the roles of toll-like receptor 4 in propofol-caused suppression of tumor necrosis factor-alpha (TNF-alpha) biosynthesis in LPS-stimulated macrophages and its possible molecular mechanisms. Exposure of macrophages to propofol and LPS did not affect cell viability. Meanwhile, the LPS-caused augmentations in the productions of TNF-alpha protein and mRNA were significantly decreased following incubation with a therapeutic concentration of propofol (50 microM). Analysis of toll-like receptor 4 small interference (si)RNA revealed that this membrane receptor might participate in the propofol-caused suppression of TNF-alpha biosynthesis. Treatment of macrophages with LPS-induced toll-like receptor 4 protein and mRNA productions. Propofol at a clinically relevant concentration could inhibit such induction. In parallel, the LPS-induced translocation and transactivation of transcription factor nuclear factor-kappa B (NFkappaB) were significantly alleviated following propofol incubation. There are several NFkappaB DNA-binding motifs found in the promoter region of toll-like receptor 4. Therefore, this study shows that propofol at a therapeutic concentration can downregulate TNF-alpha biosynthesis possibly via inhibition of NFkappaB-mediated toll-like receptor 4 gene expression. ------>tmu_sno=None ------>sno=21919 ------>authors2=Chen TL ------>authors3=Chang CC ------>authors4=Chen RM ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Wu GJ ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Propofol suppresses tumor necrosis factor-alpha biosynthesis in lipopolysaccharide-stimulated macrophages possibly through downregulation of nuclear factor-kappa B-mediated toll-like receptor 4 gene expression. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=7 |