title: Salidroside protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via PI3K-Akt dependent pathway.
abstract: Oxidative stress induces serious tissue injury in cardiovascular diseases. Salidroside, with its strong antioxidative and cytoprotective actions, is of particular interest in the development of antioxidative therapies for oxidative injury in cardiac diseases. We examined the pharmacological effects of salidroside on H9c2 rat cardiomyoblast cells under conditions of oxidative stress induced by hydrogen peroxide (H2O2) challenge. Salidroside attenuated H2O2-impaired cell viability in a concentration-dependent manner, and effectively inhibited cellular malondialdehyde production, lethal sarcolemmal disruption, cell necrosis, and apoptosis induced by H2O2 insult. Salidroside significantly augmented Akt phosphorylation at Serine 473 in the absence or presence of H2O2 stimulation; wortmannin, a specific inhibitor of PI3K, abrogated salidroside protection. Salidroside increased the intracellular mRNA expression and activities of catalase and Mn-superoxide dismutases in a PI3K-dependent manner. Our results indicated that salidroside protected cardiomyocytes against oxidative injury through activating the PI3K/Akt pathway and increasing the expression and activities of endogenous PI3K dependent antioxidant enzymes.
authors.affiliation: Department of Cardiology, Molecular Medicine Research Center, State Key Laboratory, West China Hospital, Sichuan University, Chengdu, Sichuan, PR China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Zhu
authors.forename: Ya-Ping
authors.initials: YP
authors.lastname: Shi
authors.forename: Dan
authors.initials: D
authors.lastname: Wu
authors.forename: Ya-Jing
authors.initials: YJ
authors.lastname: Ji
authors.forename: Xue
authors.initials: X
authors.lastname: Wang
authors.forename: Hua-Li
authors.initials: HL
authors.lastname: Chen
authors.forename: Si-Si
authors.initials: SS
authors.lastname: Wu
authors.forename: De-Jia
authors.initials: DJ
authors.lastname: Huang
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
mesh_terms: D000730:Androstadienes / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D019610:Cytoprotection; D005434:Flow Cytometry; D015870:Gene Expression; D005960:Glucosides / Q000494:pharmacology*; D006861:Hydrogen Peroxide / Q000009:adverse effects / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000032:analysis; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology; D018384:Oxidative Stress / Q000187:drug effects*; D010636:Phenols / Q000494:pharmacology*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation; D016133:Polymerase Chain Reaction; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D000975:Antioxidants; D005960:Glucosides; D006861:Hydrogen Peroxide; D008315:Malondialdehyde; D010636:Phenols; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; D000077191:Wortmannin; C009172:rhodioloside