title: Effects of Salidroside on Myocardial Injury In Vivo In Vitro via Regulation of Nox/NF-κB/AP1 Pathway.
abstract: Salidroside (Sal), a phenylpropanoid glycoside isolated from a popular traditional Chinese medicinal plant Rhodiola rosea L., possesses multiple pharmacological actions. This aim of this study is to investigate the effects of Sal against isoproterenol (ISO)-induced myocardial ischemia. Fifty male Sprague-Dawley rats were randomized equally to five groups: control group, ISO group, Sal (20 mg/kg; 40 mg/kg) treatments groups, and propranolol (Pro, 15 mg/kg) group. Rats were treated for 14 days and then given ISO (80 mg/kg) for 2 consecutive days by subcutaneous injection. In vitro, we used H9C2 cells to investigate the effects of Sal against hypoxia-reoxygenation. ST-segment elevation was measured after the last administration. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and malondialdehyde (MDA); levels of NADPH oxidases 2 and 4 (Nox2 and Nox4), NF-κBP65, and AP1 in heart, and H9C2 cells were measured by Western blot. The hearts were excised for determining microscopic examination, SOD, and MDA measurements. Sal decreased the ST elevation induced by ISO, decreased serum levels of CK-MB, LDH, TNF-α, IL-6, SOD, and MDA. In addition, Sal increased SOD activity and decreased MDA content in myocardial tissue. Sal also decreased Nox2 and 4, NF-κBP65, P-NF-κBP65, and AP1 protein levels in the heart. The results support a further study of Sal as potential treatments for ischemic heart disease.
authors: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
authors: Lingpeng
authors: L
authors: Zhu
authors: Tingting
authors: T
authors: Wei
authors: Xiayun
authors: X
authors: Chang
authors: He
authors: H
authors: He
authors: Jin
authors: J
authors: Gao
authors: Zhengli
authors: Z
authors: Wen
authors: Tianhua
authors: T
authors: Yan
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005960:Glucosides / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000502:physiology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000502:physiology*; D010636:Phenols / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D018808:Transcription Factor AP-1 / Q000037:antagonists & inhibitors / Q000502:physiology*; D016896:Treatment Outcome
chemical_list: D005960:Glucosides; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D010636:Phenols; D018808:Transcription Factor AP-1; C500593:Cybb protein, rat; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases; C009172:rhodioloside