, Volume 38, Issue 6, pp 2178–2184 | Cite as

Salidroside Mitigates Sepsis-Induced Myocarditis in Rats by Regulating IGF-1/PI3K/Akt/GSK-3β Signaling

  • He He
  • Xiayun Chang
  • Jin Gao
  • Lingpeng Zhu
  • Mingxing Miao
  • Tianhua Yan


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.


salidroside sepsis myocardial inflammation IGF-I/PI3K/Akt/GSK-3β signaling 



This work was supported by the National Twelve Five Major Drug Discovery Project (2011ZX09102-002-01).


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© Springer Science+Business Media New York 2015

Authors and Affiliations

  1. 1.Department of Physiology and PharmacologyChina Pharmaceutical UniversityNanjingChina

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