title: Salidroside Mitigates Sepsis-Induced Myocarditis in Rats by Regulating IGF-1/PI3K/Akt/GSK-3β Signaling.
abstract: Sepsis-induced myocardial injury (SIMI) is caused by various mechanisms. The aim of this study was to investigate the effects of salidroside (Sal) on SIMI and its mechanisms in rats. The sepsis model was established by intraperitoneal injection of lipopolysaccharide (LPS) (15 mg/kg in sterile saline). Sal decreased the serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), whereas the expressions of insulin-like growth factor-1 (IGF-1) signaling-related proteins, such as IGF-1 and its corresponding receptor (IGF-1R), phosphatidylinositol 3-kinase (PI3K), p-PI3K, Akt, p-Akt, and glycogen synthase kinase-3β (GSK-3β), in the heart were decreased with Sal pretreatment. Mitigated myocardial cell swelling, degeneration, loss of transverse striations, and inflammatory cell infiltration were also observed in the LPS + Sal groups. Thus, Sal is assumed to exert pronounced cardioprotective effects in rats subjected to LPS, probably through regulation of IGF-1/PI3K/Akt/GSK-3β signaling.
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
authors.forename: He
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
authors.forename: Xiayun
authors.initials: X
authors.lastname: Chang
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
authors.forename: Lingpeng
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China. miaomingxingcpu@126.com.
authors.forename: Mingxing
authors.initials: M
authors.lastname: Miao
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China. yantianhuabest@126.com.
authors.forename: Tianhua
authors.initials: T
authors.lastname: Yan
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D005960:Glucosides / Q000494:pharmacology*; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism*; D000071679:Glycogen Synthase Kinase 3 beta; D018836:Inflammation Mediators / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008070:Lipopolysaccharides; D008297:Male; D009205:Myocarditis / Q000097:blood / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D010636:Phenols / Q000494:pharmacology*; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005960:Glucosides; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D010636:Phenols; C548904:insulin-like growth factor-1, rat; C482199:lipopolysaccharide, E coli O55-B5; D007334:Insulin-Like Growth Factor I; D058539:Phosphatidylinositol 3-Kinase; D000071679:Glycogen Synthase Kinase 3 beta; C000605508:Gsk3b protein, rat; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3; C009172:rhodioloside
keywords: IGF-I/PI3K/Akt/GSK-3β signaling; myocardial inflammation; salidroside; sepsis