title: Effects of ginsenoside on pacemaker potentials of cultured interstitial cells of Cajal clusters from the small intestine of mice.
abstract: Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiological and pharmacological actions in various organs. However, little is known about the effects of ginsenosides on gastrointestinal (GI) motility. We studied the modulation of pacemaker potentials by ginsenoside in the interstitial cells of Cajal (ICCs) using the whole-cell patch clamp technique in the current clamp mode. Among ginsenosides, we investigated the effects of ginsenoside Rb1, Rg3 and Rf. While externally applied Rb1 and Rg3 had no effects on pacemaker potentials, Rf caused membrane depolarization. The application of flufenamic acid or niflumic acid abolished the generation of pacemaker potentials and inhibited the Rf-induced membrane depolarization. Membrane depolarization induced by Rf was not inhibited by intracellular application of guanosine 5'-[β-thio]diphosphate trilithium salt. Pretreatment with a Ca(2+)-free solution, thapsigargin, a Ca(2+)-ATPase inhibitor of the endoplasmic reticulum, U-73122, a phospholipase C inhibitor, or 2-APB, an IP3 receptor inhibitor, abolished the generation of pacemaker potentials and suppressed Rfinduced actions. However, treatment with chelerythrine and calphostin C, protein kinase C inhibitors, did not block Rf-induced effects on pacemaker potentials. These results suggest that ginsenoside Rf modulates the pacemaker activities of ICCs and thereby regulates intestinal motility.
authors.affiliation: Division of Longevity and Biofunctional Medicine, Pusan National University School of Korean Medicine, Yangsan 626-870, Korea.
authors.forename: Seungheon
authors.initials: S
authors.lastname: Han
authors.forename: Jung Soo
authors.initials: JS
authors.lastname: Kim
authors.forename: Bo Kyoung
authors.initials: BK
authors.lastname: Jung
authors.forename: Song Ee
authors.initials: SE
authors.lastname: Han
authors.forename: Joo Hyun
authors.initials: JH
authors.lastname: Nam
authors.forename: Young Kyu
authors.initials: YK
authors.lastname: Kwon
authors.forename: Seung-Yeol
authors.initials: SY
authors.lastname: Nah
authors.forename: Byung Joo
authors.initials: BJ
authors.lastname: Kim
mesh_terms: D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001683:Biological Clocks / Q000187:drug effects*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002478:Cells, Cultured; D018118:Chloride Channels / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005439:Flufenamic Acid / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors; D005769:Gastrointestinal Motility / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology*; D006153:Guanosine Diphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D056885:Interstitial Cells of Cajal / Q000187:drug effects* / Q000502:physiology; D007421:Intestine, Small / Q000166:cytology*; D008297:Male; D049990:Membrane Transport Modulators / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D009544:Niflumic Acid / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D050053:TRPM Cation Channels / Q000378:metabolism; D013873:Thionucleotides / Q000494:pharmacology; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors
chemical_list: D018118:Chloride Channels; D004791:Enzyme Inhibitors; D036145:Ginsenosides; D049990:Membrane Transport Modulators; D050053:TRPM Cation Channels; D013873:Thionucleotides; D006153:Guanosine Diphosphate; D009544:Niflumic Acid; D005439:Flufenamic Acid; C023427:guanosine 5'-O-(2-thiodiphosphate); C421903:Trpm7 protein, mouse; D011493:Protein Kinase C; D010738:Type C Phospholipases; D019204:GTP-Binding Proteins; D000252:Calcium-Transporting ATPases