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Lipopolysaccharide-induced myocardial protection against ischaemia/reperfusion injury is mediated through a PI3K/Akt-dependent mechanism

机译:脂多糖诱导的心肌对缺血/再灌注损伤的保护作用是通过PI3K / Akt依赖性机制介导的

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Aims The ability of lipopolysaccharide (LPS) pre-treatment to induce cardioprotection following ischaemia/reperfusion (I/R) has been well documented; however, the mechanisms have not been fully elucidated. LPS is a Toll-like receptor 4 (TLR4) ligand. Recent evidence indicates that there is cross-talk between the TLR and phosphoinositide 3-kinase/Akt (PI3K/Akt) signalling pathways. We hypothesized that activation of PI3K/Akt signalling plays a critical role in LPS-induced cardioprotection.
机译:目的脂多糖(LPS)预处理在缺血/再灌注(I / R)后诱导心脏保护的能力已得到充分证明;但是,机制尚未完全阐明。 LPS是Toll样受体4(TLR4)配体。最近的证据表明,TLR和磷酸肌醇3-激酶/ Akt(PI3K / Akt)信号通路之间存在串扰。我们假设PI3K / Akt信号的激活在LPS诱导的心脏保护中起关键作用。

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