title: Salvianolic acid A demonstrates cardioprotective effects in rat hearts and cardiomyocytes after ischemia/reperfusion injury.
abstract: Salvianolic acid A (Sal A), the water-soluble component from the root of the Salvia miltiorrhiza plant, possesses antioxidant, antiproliferative, and antiplatelet properties. However, whether it plays a role in the protection against ischemia-reperfusion (I/R) injury in rat hearts has yet to be elucidated. In the present study, we tested cell viability, shortening amplitude, necrosis, apoptosis, and the expression levels of Akt, phosphorylated Akt, Bcl-2, Bax, and caspase-3 after 3-hour simulated ischemia and 2- or 6-hour simulated reperfusion in cardiomyocytes. We further observed the contractile function and infarct size in isolated hearts after they were subjected to global 30-minute ischemia and 120-minute reperfusion. Pretreatment with Sal A markedly increased cell viability and shortening amplitude while reducing evidence of necrosis and apoptosis in the cells. In addition, the expression of Bcl-2 was upregulated and Bax was downregulated, thereby increasing the Bcl-2/Bax ratio. Sal A inhibited the activation of caspase-3 as well. The results also showed that Sal A significantly increased phosphorylation of Akt and that this phosphorylation can be partially inhibited by phosphoinositide 3-kinase/Akt inhibitor. Furthermore, Sal A improved I/R-induced myocardial contractile function and reduced infarct size. In summary, our results showed that Sal A prevents I/R-induced myocardial damage by reducing necrosis and apoptosis in isolated rat hearts and cardiomyocytes.
authors.affiliation: Research Institute of Cardiovascular Disease, Xuzhou Medical College, Xuzhou, Jiangsu, China.
authors.forename: Huanjun
authors.initials: H
authors.lastname: Pan
authors.forename: Dongye
authors.initials: D
authors.lastname: Li
authors.forename: Fang
authors.initials: F
authors.lastname: Fang
authors.forename: Dan
authors.initials: D
authors.lastname: Chen
authors.forename: Lingling
authors.initials: L
authors.lastname: Qi
authors.forename: Ruiqu
authors.initials: R
authors.lastname: Zhang
authors.forename: Tongda
authors.initials: T
authors.lastname: Xu
authors.forename: Hong
authors.initials: H
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002109:Caffeic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D053148:Caspase 3 / Q000378:metabolism; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D007773:Lactates / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000473:pathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009336:Necrosis / Q000473:pathology / Q000517:prevention & control; D010477:Perfusion; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000517:prevention & control; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D002109:Caffeic Acids; D002316:Cardiotonic Agents; D007773:Lactates; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C066201:salvianolic acid A; D007770:L-Lactate Dehydrogenase; D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3