title: Protective effects of Millettia pulchra flavonoids on myocardial ischemia in vitro and in vivo.
abstract: BACKGROUND
  Previous studies have demonstrated that Millettia pulchra flavonoids (MPF) exhibit protective effects on myocardial ischemia reperfusion injury (MI/RI) in isolated rat hearts and show anti-oxidative, anti-hypoxic and anti-stress properties.
  
  
  METHODS
  In this study, the cardioprotective effects of MPF on myocardial ischemia and its underlying mechanisms were investigated by a hypoxia/ reoxygenation (H/R) injury model in vitro and a rat MI/RI model in vivo.
  
  
  RESULTS
  We found that the lactate dehydrogenase (LDH) and inducible nitric oxide synthase (iNOS) activities were decreased in the MPF pretreatment group, whereas the activities of constructional nitric oxide synthase (cNOS), total nitric oxide synthase (tNOS), Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase were significantly increased. In addition, the cardiocytes were denser in the MPF groups than in the control group. The mortality rate and apoptosis rate of cardiocytes were significantly decreased. Furthermore, pretreatment with MPF in vivo significantly improved the hemodynamics, decreased malondialdehyde (MDA) abundance, increased the activities of plasma superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the expression of the Bax protein and ratio Bax/Bc1-2 ration.
  
  
  CONCLUSIONS
  These results suggest that MPF is an attractive protective substance in myocardial ischemia due to its negative effects on heart rate and ionotropy, reduction of myocardial oxidative damage and modulation of gene expression associated with apoptosis.
authors.affiliation: Department of Pharmacology, Guangxi Medical University, Nanning, PR China.
authors.forename: Jianchun
authors.initials: J
authors.lastname: Huang
authors.forename: Xudong
authors.initials: X
authors.lastname: Zhang
authors.forename: Feizhang
authors.initials: F
authors.lastname: Qin
authors.forename: Yingxin
authors.initials: Y
authors.lastname: Li
authors.forename: Xiaoqun
authors.initials: X
authors.lastname: Duan
authors.forename: Jie
authors.initials: J
authors.lastname: Jian
authors.forename: Yongwen
authors.initials: Y
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Renbin
authors.initials: R
authors.lastname: Huang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D005419:Flavonoids / Q000008:administration & dosage* / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects*; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D033641:Millettia / Q000737:chemistry*; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D005419:Flavonoids; D007770:L-Lactate Dehydrogenase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat