Glutamine ameliorates lipopolysaccharide‑induced cardiac dysfunction by regulating the toll‑like receptor 4/mitogen‑activated protein kinase/nuclear factor‑κB signaling pathway
- Wen‑Bin Zhang
- Hai‑Yue Zhang
- Qian Zhang
- Fang‑Zhou Jiao
- Hong Zhang
- Lu‑Wen Wang
- Zuo‑Jiong Gong
Published online on: October 17, 2017
Copyright: © Zhang et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
The inflammatory response of sepsis induced by lipopolysaccharide (LPS) may result in irreversible cardiac dysfunction. Glutamine (GLN) has a multitude of pharmacological effects, including anti‑inflammatory abilities. Previous studies have reported that GLN attenuated LPS‑induced acute lung injury and intestinal mucosal injury. The present study investigated whether GLN exerts potential protective effects on LPS‑induced cardiac dysfunction. Male Sprague‑Dawley rats were divided into three groups (15 rats per group), including the control (saline‑treated), LPS and LPS+GLN groups. Pretreatment with 1 g/kg GLN was provided via gavage for 5 days in the LPS+GLN group, while the control and LPS groups received the same volume of normal saline. On day 6, a cardiac dysfunction model was induced by administration of LPS (10 mg/kg). After 24 h, the cardiac functions of the rats that survived were detected by echocardiography and catheter‑based measurements. The serum levels of tumor necrosis factor α (TNF‑α), interleukin (IL)‑1β and IL‑6 were detected by enzyme‑linked immunosorbent assay, while the mRNA levels of toll‑like receptor (TLR)4, TNF‑α, IL‑1β and IL‑6 were examined by reverse transcription‑quantitative polymerase chain reaction. The protein expression of TLR4, mitogen‑activated protein kinase (MAPK) and nuclear factor‑κB (NF‑κB) were also determined by western blot analysis. The results of echocardiography and catheter‑based measurements revealed that GLN treatment attenuated cardiac dysfunction. GLN treatment also attenuated the serum and mRNA levels of the pro‑inflammatory cytokines. In addition, the protein levels of TLR4, phosphorylated (p‑)extracellular signal‑regulated kinase, p‑c‑Jun N‑terminal kinase and p‑P38 were reduced upon GLN pretreatment. Furthermore, GLN pretreatment resulted in decreased activation of the NF‑κB signaling pathway. In conclusion, GLN has a potential therapeutic effect in the protection against cardiac dysfunction mediated by sepsis through regulating the TLR4/MAPK/NF‑κB signaling pathway.