| Yu-Ti Chen |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=6.499 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=shtsai ------>insert_bywho=shtsai ------>Jurnal_Rank=3.8 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=3 ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=J0600 ------>insert_date=20091014 ------>iam=2 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Stroke ------>paper_name=Ghrelin improves lipopolysaccharide-induced gastrointestinal motility disturbances: roles of nitric oxide and prostaglandin E2. ------>confirm_date=20091015 ------>tch_id=089089 ------>pmid=19503023 ------>page1= ------>fullAbstract=Ghrelin, an important orexigenic peptide, exerts gastroprokinetic and anti-inflammatory effects. We investigated the role of ghrelin in lipopolysaccharide (LPS)-induced gastrointestinal (GI) motility disturbances through nitric oxide (NO) and prostaglandin E2 (PGE2) pathways in mice. Ghrelin-containing cells and its receptor-growth hormone secretagogue receptor-1 (GHS-R1) were localized in the stomach and duodenum using an immunohistochemical method. The distribution of ghrelin-containing cells or GHS-R1 immunoreactivity in both the mucosal and muscle layers was heterogeneous within both tissues. The intraperitoneal (I.p.) administration of ghrelin (1~20 mug/kg) had no effect on gastric emptying, but markedly increased the GI transit (GIT) in normal mice. LPS (20 mg/kg; I.p.)-treated mice showed significant decreases in the gastric emptying and GIT. Ghrelin attenuated the LPS-induced delay in gastric emptying and GIT. We also performed immunohistochemical experiments on both tissues. Immunohistochemistry showed the presence of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 in both tissues of LPS-treated mice. Treatment of LPS-exposed mice with ghrelin (20 mug/kg) diminished the presence of iNOS but not COX-2 in both tissues. The effect of ghrelin on regulating LPS-induced GI motility disturbance was further found to be associated with a reduction in iNOS expression in the GI tract and plasma NO overproduction rather than regulation of neural (n)NOS or endothelial (e)NOS expression in the GI tissue. In addition, ghrelin was found to elevate PGE2 levels in the GI tissue but showed no significant change in LPS-treated mice.These findings indicate that the action of ghrelin binding to GHS-R1 improves endotoxemia-induced GI motility disturbances mainly through down regulating the NO pathway in the GI tract. ------>tmu_sno=None ------>sno=22653 ------>authors2=Shin-Han Tsai ------>authors3=Shiow-Yunn Sheu ------>authors4=Li Hsueh Tsai ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Yu-Ti Chen ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Ghrelin improves lipopolysaccharide-induced gastrointestinal motility disturbances: roles of nitric oxide and prostaglandin E2. ------>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=6 |