title: Electrophysiological effects of anthopleurin-Q on rat hepatocytes.
abstract: OBJECTIVE
  To study the effects of AP-Q on CCl(4)-induced acute liver injury, delayed outward potassium current (I(K)), inward rectifier potassium current (I(K1)) and calcium release-activated calcium current (I(CRAC)) in isolated rat hepatocytes.
  
  
  METHODS
  A single dose of CCl(4) (10 microg/mL, ip) was injected to induce acute liver injury in rats. Serum aminotransferase activities were determined. Whole cell patch-clamp techniques were used to investigate the effects of AP-Q on delayed outward potassium current (I(K)), inward rectifier potassium current (I(K1)) and calcium release-activated calcium current (I(CRAC)).
  
  
  RESULTS
  AP-Q (3.5 and 7 microg/kg) pretreatment significantly reduced ALT and AST activities. AP-Q 0.1-100 nM produced a concentration-dependent increase of I(K) with EC(50) value of 5.55+/-1.8 nM (n=6). AP-Q 30 nM shifted the I-V curve of I(K) leftward and upward. CCl(4) 4 mM decreased I(K) current 28.6+/-6.5% at 140 mV. After exposure to CCl(4) for 5 min, AP-Q 30 nM attenuated the decrease of I(K) induced by CCl(4) close to normal amplitude. AP-Q 0.01-100 nM had no significant effect on either inward or outward components of I(K1) at any membrane potential examined. AP-Q 0.1-100 nM had no significant influence on the peak amplitude of I(CRAC), either, and did not affect the shape of its current voltage curve.
  
  
  CONCLUSIONS
  AP-Q has a protective effect on CCl(4)-induced liver injury, probably through selectively increased I(K) in hepatocytes.
authors.affiliation: Department of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China. zhouhy518@yahoo.com.cn
authors.forename: Hong-Yi
authors.initials: HY
authors.lastname: Zhou
authors.forename: Fang
authors.initials: F
authors.lastname: Wang
authors.forename: Ke-Qiang
authors.initials: KQ
authors.lastname: Zhang
authors.forename: Lan
authors.initials: L
authors.lastname: Cheng
authors.forename: Ji
authors.initials: J
authors.lastname: Zhou
authors.forename: Li-Ying
authors.initials: LY
authors.lastname: Fu
authors.forename: Wei-Xing
authors.initials: WX
authors.lastname: Yao
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury; D005260:Female; D022781:Hepatocytes / Q000187:drug effects* / Q000502:physiology*; D036341:Intercellular Signaling Peptides and Proteins; D008107:Liver Diseases / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008815:Mice, Inbred Strains; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015220:Calcium Channels; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D024661:Potassium Channels, Inwardly Rectifying; C477842:anthopleurin-Q; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D011188:Potassium; D002118:Calcium