title: Arctigenin, a potential anti-arrhythmic agent, inhibits aconitine-induced arrhythmia by regulating multi-ion channels.
abstract: OBJECTIVE
  Arctigenin possesses biological activities, but its underlying mechanisms at the cellular and ion channel levels are not completely understood. Therefore, the present study was designed to identify the anti-arrhythmia effect of arctigenin in vivo, as well as its cellular targets and mechanisms.
  
  
  METHODS
  A rat arrhythmia model was established via continuous aconitine infusion, and the onset times of ventricular premature contraction, ventricular tachycardia and death were recorded. The Action Potential Duration (APD), sodium current (I(Na)), L-type calcium current (I(Ca, L)) and transient outward potassium current (I(to)) were measured and analysed using a patch-clamp recording technique in normal rat cardiomyocytes and myocytes of arrhythmia aconitine-induced by.
  
  
  RESULTS
  Arctigenin significantly delayed the arrhythmia onset in the aconitine-induced rat model. The 50% and 90% repolarisations (APD50 and APD90) were shortened by 100 µM arctigenin; the arctigenin dose also inhibited the prolongation of APD50 and APD90 caused by 1 µM aconitine. Arctigenin inhibited I(Na) and I(Ca,L) and attenuated the aconitine-increased I(Na) and I(Ca,L) by accelerating the activation process and delaying the inactivation process. Arctigenin enhanced Ito by facilitating the activation process and delaying the inactivation process, and recoverd the decreased Ito induced by aconitine.
  
  
  CONCLUSIONS
  Arctigenin has displayed anti-arrhythmia effects, both in vivo and in vitro. In the context of electrophysiology, I(Na), I(Ca, L), and I(to) may be multiple targets of arctigenin, leading to its antiarrhythmic effect.
authors.affiliation: College of Pharmacy, Nankai University, Tianjin, P.R. China.
authors.forename: Zhenying
authors.initials: Z
authors.lastname: Zhao
authors.forename: Yongqiang
authors.initials: Y
authors.lastname: Yin
authors.forename: Hong
authors.initials: H
authors.lastname: Wu
authors.forename: Min
authors.initials: M
authors.lastname: Jiang
authors.forename: Jianshi
authors.initials: J
authors.lastname: Lou
authors.forename: Gang
authors.initials: G
authors.lastname: Bai
authors.forename: Guo'an
authors.initials: G
authors.lastname: Luo
mesh_terms: D000157:Aconitine / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D005663:Furans / Q000494:pharmacology*; D007473:Ion Channels / Q000378:metabolism*; D017705:Lignans / Q000494:pharmacology*; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D018408:Patch-Clamp Techniques / Q000379:methods; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000378:metabolism
chemical_list: D000889:Anti-Arrhythmia Agents; D020746:Calcium Channels, L-Type; D005663:Furans; D007473:Ion Channels; D017705:Lignans; D015221:Potassium Channels; D015222:Sodium Channels; C071942:arctigenin; D000157:Aconitine