title: [Auricularia auricular polysaccharide protects myocardium against ischemia/reperfusion injury].
abstract: OBJECTIVE
  To determine whether auricularia auricular polysaccharide (AAP) protects heart against ischemia/reperfusion (1/ R) injury and its underlying mechanisms.
  
  
  METHODS
  Male Sprague-Dawley rats, pretreated with AAP (50, 100, 200 mg/(kg x d), gastric perfusion) for 4 weeks, were used for Langendorff isolated heart perfusion. The hearts were subjected to global ischemia for 30 min followed by 120 min of reperfusion and the left ventricular hemodynamic parameters were measured. Formazan, a product of 2, 3, 5-triphenyl-tetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. The cardiac malondialdehyde (MDA), a product of lipid peroxidation, and superoxide dismutase (SOD) activity were determined after myocardial I/R.
  
  
  RESULTS
  The pretreatment with AAP at 50, 100, 200/(kg d) for 4 weeks before I/R increased myocardial formazan content, reduced LDH release, improved the recovery of the left ventficular developed pressure, maximal rise rate of left ventricular pressure, and rate pressure product (left ventricular developed pressure multiplied by heart rate) attenuated the decrease of coronary flow during reperfusion. The cardiac protective effect of high dose AAP was more potent than that of compound radix salviae miltiorrhizae (CRSM, 4 ml/(kg x d), gastric perfusion for 4 weeks). Pretreatment with AAP (100 mg/(kg x d)) markedly inhibited the increase of MDA level and the decrease of SOD activity induced by I/R in myocardium.
  
  
  CONCLUSIONS
  The findings indicate that in the isolated rat heart, AAP protects myocardium against ischemia/reperfusion injury via enhancing the activity of SOD and reducing lipid peroxidation in heart.
authors.affiliation: Department of Biology, College of Chemistry and Life Sciences, Lishui University, China.
authors.forename: Ting-mei
authors.initials: TM
authors.lastname: Ye
authors.forename: Ling-bo
authors.initials: LB
authors.lastname: Qian
authors.forename: Jie
authors.initials: J
authors.lastname: Cui
authors.forename: Hui-ping
authors.initials: HP
authors.lastname: Wang
authors.forename: Zhi-guo
authors.initials: ZG
authors.lastname: Ye
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000818:Animals; D001487:Basidiomycota / Q000737:chemistry*; D008297:Male; D017202:Myocardial Ischemia / Q000473:pathology / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects; D011134:Polysaccharides / Q000302:isolation & purification / Q000494:pharmacology*; D020011:Protective Agents / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D011134:Polysaccharides; D020011:Protective Agents; D013482:Superoxide Dismutase