| Literature DB >> 26104971 |
He He1, Xiayun Chang1, Jin Gao1, Lingpeng Zhu1, Mingxing Miao2, Tianhua Yan3.
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.Entities:
Keywords: IGF-I/PI3K/Akt/GSK-3β signaling; myocardial inflammation; salidroside; sepsis
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Year: 2015 PMID： 26104971 DOI： 10.1007/s10753-015-0200-7
Source DB: PubMed Journal: Inflammation ISSN： 0360-3997 Impact factor: 4.092