| Lin CH |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=1.718 ------>paper_class3=2 ------>paper_class2=1 ------>vol=54 ------>confirm_bywho=amel ------>insert_bywho=llyang ------>Jurnal_Rank=61.0 ------>authors4_c= ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=1278 ------>medlineContent= ------>unit=G0100 ------>insert_date=20081215 ------>iam=5 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN=0022-3573 ------>authors_c= ------>score=500 ------>journal_name=J Pharm Pharmacol. ------>paper_name=Byakangelicol, isolated from Angelica dahurica, inhibits both the activity and induction of cyclooxygenase-2 in human pulmonary epithelial cells ------>confirm_date=20081217 ------>tch_id=058001 ------>pmid=12356282 ------>page1=1271 ------>fullAbstract=We examined the inhibitory mechanism of byakangelicol, isolated from Angelica dahurica, on interleukin-1beta (IL-1beta)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human pulmonary epithelial cell line (A549). Byakangelicol (10-50 microM) concentration-dependently attenuated IL-1beta-induced COX-2 expression and PGE2 release. The selective COX-2 inhibitor, NS-398 (0.01-1 microM), and byakangelicol (10-50 microM) both concentration-dependently inhibited the activity of the COX-2 enzyme. Byakangelicol, at a concentration up to 200 microM, did not affect the activity and expression of COX-1 enzyme. IL-1beta-induced p44/42 mitogen-activated protein kinase (MAPK) activation was inhibited by the MAPK/extracellular signal-regulated protein kinase (MEK) inhibitor, PD 98059 (30 microM), while byakangelicol (50 microM) had no effect. Treatment of cells with byakangelicol (50 microM) or pyrrolidine dithiocarbamate (PDTC; 50 microM) partially inhibited IL-1beta-induced degradation of IkappaB-alpha in the cytosol, translocation of p65 NF-kappaB from the cytosol to the nucleus and the NF-kappaB-specific DNA-protein complex formation. Taken together, we have demonstrated that byakangelicol inhibits IL-1beta-induced PGE2 release in A549 cells; this inhibition may be mediated by suppression of COX-2 expression and the activity of COX-2 enzyme. The inhibitory mechanism of byakangelicol on IL-1beta-induced COX-2 expression may be, at least in part, through suppression of NF-kappaB activity. Therefore, byakangelicol may have therapeutic potential as an anti-inflammatory drug on airway inflammation. ------>tmu_sno=None ------>sno=20841 ------>authors2=Chang CW ------>authors3=Wang CC ------>authors4=Chang MS ------>authors5=Yang LL ------>authors6= ------>authors6_c= ------>authors=Lin CH ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Byakangelicol, isolated from Angelica dahurica, inhibits both the activity and induction of cyclooxygenase-2 in human pulmonary epithelial cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=9 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2002 ------>submit_flag=None ------>publish_month=9 |