title: [Effects of Guanxinkang on expressions of ATP-sensitive potassium channel subunits Kir6.1, Kir6.2, SUR2A and SUR2B in ischemic myocytes of rats].
abstract: OBJECTIVE
  To observe the effects of Guanxinkang injection, a compound traditional Chinese herbal medicine, on ATP-sensitive potassium (K(ATP)) channel subunits in ischemic myocardial cells of rats, and to explore the mechanism of Guanxinkang in protecting myocardial ischemic reperfusion injuries.
  
  
  METHODS
  Forty-eight Wistar rats were randomly divided into normal group, untreated group, glibenclamide group, pinacidil group, Guanxinkang group and Guanxinkang plus glibenclamide group. The ventricular myocytes were prepared from hearts of normal rats by enzymatic dissociation method. The ischemic ventricular myocytes underwent perfusion with normal Tyrode solution for 10 min, then stopping perfusion 30 min, and followed by 45 min of reperfusion. The glibenclamide, pinacidil and Guanxinkang were added into ventricular myocytes solution directly. Then the solutions were placed at 4 degrees centigrade. After 24-hour freezing at -80 degrees centigrade, mRNA and protein expressions of KATP subunits Kir6.1, Kir6.2, SUR2A and SUR2B were measured by real-time quantitative polymerase chain reaction and Western blotting respectively.
  
  
  RESULTS
  In normal rat myocardial cells, there were SUR2A, Kir6.1, and Kir6.2 protein and gene expressions but no expression of SUR2B protein. In the untreated group, all subunit mRNA and protein expressions of KATP increased to some extent as compared with the normal group. Pinacidil, a potassium channel opener, significantly increased mRNA and protein expressions of KATP subunits, while the blocker glibenclamide had a reverse effect. Meanwhile, Guanxinkang injection significantly increased mRNA and protein expressions of K(ATP) subunits but with no significant difference as compared with pinacidil.
  
  
  CONCLUSIONS
  Guanxinkang injection can obviously enhance the open of KATP channel and thus play a role in cardiovascular protection.
authors.affiliation: Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
authors.forename: Fu-rong
authors.initials: FR
authors.lastname: Chen
authors.forename: Na
authors.initials: N
authors.lastname: Zhang
authors.forename: Ping
authors.initials: P
authors.lastname: Liu
authors.forename: Yi-yi
authors.initials: YY
authors.lastname: Zhang
authors.forename: Xiang-hui
authors.initials: XH
authors.lastname: Han
authors.forename: Jue-feng
authors.initials: JF
authors.lastname: Cai
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000378:metabolism*; D000818:Animals; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D054086:KATP Channels / Q000378:metabolism*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011955:Receptors, Drug / Q000378:metabolism*; D064233:Sulfonylurea Receptors; D000099161:Kcnj11 Channel
chemical_list: D018528:ATP-Binding Cassette Transporters; D004365:Drugs, Chinese Herbal; D054086:KATP Channels; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; D064233:Sulfonylurea Receptors; D000099161:Kcnj11 Channel; C092520:uK-ATP-1 potassium channel