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首页> 外文期刊>Endocrinology >Insulin-like growth factor and epidermal growth factor treatment: new approaches to protecting steatotic livers against ischemia-reperfusion injury.
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Insulin-like growth factor and epidermal growth factor treatment: new approaches to protecting steatotic livers against ischemia-reperfusion injury.

机译：胰岛素样生长因子和表皮生长因子的治疗：保护脂肪肝免受缺血-再灌注损伤的新方法。

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摘要

Hepatic steatosis is a major risk factor in ischemia-reperfusion (I/R). IGF-binding proteins (IGFBPs) modulate IGF-I action by transporting circulating IGF-I to its sites of action. Epidermal growth factor (EGF) stimulates IGF-I synthesis in vitro. We examined the effect of IGF-I and EGF treatment, separately or in combination, on the vulnerability of steatotic livers to I/R. Our results indicated that I/R impaired IGF-I synthesis only in steatotic livers. Only when a high dose of IGF-I (400 microg/kg) was given to obese animals did they show high circulating IGF-I:IGFBP levels, increased hepatic IGF-I levels, and protection against damage. In lean animals, a dose of 100 microg/kg IGF-I protected nonsteatotic livers. Our results indicated that the combined administration of IGF-I and EGF resulted in hepatic injury parameters in both liver types similar to that obtained by IGF-I and EGF separately. IGF-I increased egf expression in both liver types. The beneficial role of EGF on hepatic I/R injury may be attributable to p38 inhibition in nonsteatotic livers and to PPAR gamma overexpression in steatotic livers. In conclusion, IGF-I and EGF may constitute new pharmacological strategies to reduce the inherent susceptibility of steatotic livers to I/R injury.
机译：肝脂肪变性是缺血再灌注（I / R）的主要危险因素。 IGF结合蛋白（IGFBP）通过将循环的IGF-I转运至其作用位点来调节IGF-I的作用。表皮生长因子（EGF）在体外刺激IGF-1合成。我们分别或联合检查了IGF-I和EGF治疗对脂肪变性肝脏对I / R脆弱性的影响。我们的结果表明，I / R仅在脂肪变性肝脏中会损害IGF-1的合成。仅当对肥胖动物给予高剂量的IGF-I（400微克/千克）时，它们才会表现出较高的循环IGF-I：IGFBP水平，增加的肝IGF-I水平以及对损伤的保护作用。在瘦动物中，以100微克/千克的IGF-I剂量保护非脂肪肝。我们的结果表明，IGF-I和EGF的联合给药导致两种肝脏类型的肝损伤参数类似于分别由IGF-I和EGF获得的肝损伤参数。 IGF-1在两种肝类型中均增加了egf表达。 EGF对肝脏I / R损伤的有益作用可能归因于非脂肪肝中p38的抑制和脂肪肝中PPARγ的过度表达。总之，IGF-I和EGF可能构成新的药理策略，以降低脂肪变性肝脏对I / R损伤的固有敏感性。

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