| Chen YU |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=2.830 ------>paper_class3=2 ------>paper_class2=1 ------>vol=377 ------>confirm_bywho=shtsai ------>insert_bywho=cck.ns ------>Jurnal_Rank=33.3 ------>authors4_c=??? ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=540 ------>medlineContent= ------>unit=J0600 ------>insert_date=20091003 ------>iam=2 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=??? ------>score=470 ------>journal_name=Naunyn-Schmiedeberg’s Archives of Pharmacology ------>paper_name=Mediation of ?-endorphin in andrographolide-induced plasma glucose-lowering action in type I diabetes-like animals. ------>confirm_date=20091005 ------>tch_id=093088 ------>pmid=18080810 ------>page1=529 ------>fullAbstract=In the present study, we investigated the mechanism(s) for glucose-lowering action of andrographolide in streptozotocin-induced diabetic rats (STZ-diabetic rats). Andrographolide lowered plasma glucose concentrations in a dose-dependent manner and increased plasma beta-endorphin-like immunoreactivity (BER) dose-dependently in diabetic rats. Both of these responses to andrographolide were abolished by the pretreatment of animals with prazosin or N-(2-(2-cyclopropylmethoxy) ethyl) 5-choro-alpha-dimethyl-1H-indole-3-thylamine (RS17053) at doses sufficient to block alpha1-adrenoceptors (ARs). Also, andrographolide enhanced BER release from isolated rat adrenal medulla in a concentration-related manner that could be abolished by alpha1-ARs antagonists. Bilateral adrenalectomy in STZ-diabetic rats eliminated the activities of andrographolide, including the plasma glucose-lowering effect and the plasma BER-elevating effect. Andrographolide failed to lower plasma glucose in the presence of opioid micro-receptor antagonists and in the opioid micro-receptor knockout diabetic mice. Treatment of STZ-diabetic rats with andrographolide resulted in the reduced expression of phosphoenolpyruvate carboxykinase (PEPCK) in liver and an increased expression of the glucose transporter subtype 4 (GLUT 4) in soleus muscle. These effects were also blocked by opioid micro-receptor antagonists. In conclusion, our results suggest that andrographolide may activate alpha1-ARs to enhance the secretion of beta-endorphin which can stimulate the opioid micro-receptors to reduce hepatic gluconeogenesis and to enhance the glucose uptake in soleus muscle, resulting in a decrease of plasma glucose in STZ-diabetic rats. However, the roles of other endogenous opioid peptides or the mixture of several opioid peptides in the activation of opioid micro-receptors associated with the plasma glucose-lowering action of andrographolide, should be considered and need more investigation in the future. ------>tmu_sno=None ------>sno=22409 ------>authors2=Chang CK ------>authors3=Su CF ------>authors4=Cheng JT ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Chen YU ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=Mediation of beta-endorphin in andrographolide-induced plasma glucose-lowering action in type I diabetes-like animals. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=4-6 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2008 ------>submit_flag=None ------>publish_month=6 |