title: The cardioprotective effect of salidroside against myocardial ischemia reperfusion injury in rats by inhibiting apoptosis and inflammation.
abstract: The main purpose of this study was to investigate effect of salidroside (Sal) on myocardial ischemia reperfusion injury in rats and the underlying mechanism. Myocardial ischemia reperfusion injury (MI/RI) model was treated with 30 min of left anterior descending (LAD) occlusion followed by 24 h of reperfusion. The male Sprague-Dawley rats were randomly divided into 7 groups: (1) Sham; (2) Sham + diltiazem (Dit, 10 mg/kg); (3) Sham + Sal (40 mg/kg); (4) I/R; (5) I/R + diltiazem (Dit, 10 mg/kg); (6) I/R + Sal (20 mg/kg); (7) I/R + Sal (40 mg/kg). Sal could ameliorate myocardial ischemia reperfusion injury as evidenced by Histopathological examination and triphenyl tetrazolium chloride (TTC) staining. Moreover, terminal deoxynucleotidyl transferase dUTP nickend labeling (TUNEL) assay demonstrated that Sal suppressed myocardial apoptosis, which may be related to up-regulation of Bcl-2/Bax ratio and inhibition of caspase-3, caspase-9 activation. Pretreatment with Sal affected serum biochemical parameters and cardiac dysfunction compared with I/R group. Sal also attenuated the pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in serum by inhibiting TLR4/NF-κB signaling pathway. Sal exerts strong favorable cardioprotective function on myocardial I/R injury which may relate to the down-regulation of the TLR4/NF-κB signaling pathway and the inhibition of cell apoptosis.
authors.affiliation: College of Life Sciences, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Lingpeng
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Wei
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Jin
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Xiayun
authors.initials: X
authors.lastname: Chang
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: He
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Fen
authors.initials: F
authors.lastname: Luo
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhou
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China. machunhuabest@126.com.
authors.forename: Chunhua
authors.initials: C
authors.lastname: Ma
authors.affiliation: College of Life Sciences, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China. liuyuyaoda@163.com.
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China. yantianhuabest@126.com.
authors.forename: Tianhua
authors.initials: T
authors.lastname: Yan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000235:genetics / Q000276:immunology; D053453:Caspase 9 / Q000235:genetics / Q000276:immunology; D005960:Glucosides / Q000008:administration & dosage*; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D010636:Phenols / Q000008:administration & dosage*; D020011:Protective Agents / Q000008:administration & dosage*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000276:immunology
chemical_list: D005960:Glucosides; D053583:Interleukin-1beta; D015850:Interleukin-6; D010636:Phenols; D020011:Protective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; D053453:Caspase 9; C009172:rhodioloside
keywords: Apoptosis; I/R injury; Inflammation; Salidroside; TLR4/NF-κB