The protection of salidroside of the heart against acute exhaustive injury and molecular mechanism in rat.
OBJECTIVE
To investigate the protection of salidroside of the heart against acute exhaustive injury and its mechanism of antioxidative stress and MAPKs signal transduction.


METHODS
Adult male SD rats were divided into four groups randomly. Cardiomyocytes ultrastructure was observed by optical microscopy and transmission electron microscopy. The contents of CK, CK-MB, LDH, MDA, and SOD were determined by ELISA method, and the phosphorylation degrees of ERK and p38 MAPK were assayed by Western blotting. Cardiac function of isolated rat heart ischemia/reperfusion was detected by Langendorff technique.


RESULTS
Salidroside reduced the myocardium ultrastructure injury caused by exhaustive swimming, decreased the contents of CK, CK-MB, and LDH, improved the LVDP, ±LV dp/dt(max) under the basic condition, reduced the content of MDA and the phosphorylation degree of p38 MAPK, and increased the content of SOD and the phosphorylation degree of ERK in acute exhaustive rats.


CONCLUSIONS
Salidroside has the protection of the heart against acute exhaustive injury. The cardioprotection is mainly mediated by antioxidative stress and MAPKs signal transduction through reducing the content of MDA, increasing the content of SOD, and increasing p-ERK and decreasing p-p38 protein expressions in rat myocardium, which might be the mechanisms of the cardioprotective effect of salidroside.
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Yunru
Y
Wang
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Peng
P
Xu
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Yang
Y
Wang
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Haiyan
H
Liu
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Yuwen
Y
Zhou
Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China.
Xuebin
X
Cao
D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D048430:Cell Shape / Q000187:drug effects; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology*; D006334:Heart Function Tests; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D010636:Phenols / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D010805:Physical Conditioning, Animal / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D002316:Cardiotonic Agents; D005960:Glucosides; D010636:Phenols; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D048049:Extracellular Signal-Regulated MAP Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D052279:Creatine Kinase, MB Form; C009172:rhodioloside