Huang YH, |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=1.837 ------>paper_class3=2 ------>paper_class2=1 ------>vol=52 ------>confirm_bywho=kueiru ------>insert_bywho=ptsai ------>Jurnal_Rank=40.9 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=535 ------>medlineContent= ------>unit=H0200 ------>insert_date=20080108 ------>iam=2 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Acta Anaesthesiol Scand ------>paper_name=Bupivacaine inhibits COX-2 expression, PGE2 and cytokine production in endotoxin-activated macrophages ------>confirm_date=20090313 ------>tch_id=091090 ------>pmid=18339158 ------>page1=530 ------>fullAbstract=BACKGROUND: Upregulation of cyclooxygenase-2 (COX-2) and resultant prostaglandin E(2) (PGE(2)) overproduction has been shown to play a crucial role in initiating a systemic inflammatory response during sepsis. Sepsis also induces robust production of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 as well as anti-inflammatory cytokine IL-10. We sought to elucidate the effects of bupivacaine on COX-2 expression and production of PGE(2) and cytokines using an endotoxin-activated murine macrophages model. METHODS: Confluent murine macrophages (RAW264.7 cells) were treated with lipopolysaccharide (LPS, 100 ng/ml) or LPS plus bupivacaine (1, 10, or 100 microM). Bupivacaine was added immediately after LPS. After reacting for 18 h, cell cultures were harvested for subsequent analysis. RESULTS: LPS significantly upregulated COX-2 transcription and PGE(2) production in macrophages. LPS also significantly increased the production of TNF-alpha, IL-1beta, IL-6 and IL-10 in macrophages. Bupivacaine significantly inhibited the effects of LPS on COX-2 transcription and PGE(2) production in a dose-dependent manner. In a dose-dependent manner, bupivacaine also significantly inhibited the effects of LPS on the production of TNF-alpha, IL-1beta, and IL-6. However, bupivacaine exerted no significant effects on LPS-induced IL-10 production. CONCLUSION: Bupivacaine significantly inhibited COX-2 expression, PGE(2) and cytokine production in endotoxin-activated macrophages. ------>tmu_sno=None ------>sno=16608 ------>authors2=Tsai PS ------>authors3=Huang CJ ------>authors4= ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Huang YH, ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Bupivacaine inhibits COX-2 expression, PGE2, and cytokine production in endotoxin-activated macrophages. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=4 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2008 ------>submit_flag=None ------>publish_month=4 |