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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Adenine nucleotide changes in the remnant liver: An early signal for regeneration after partial hepatectomy.
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Adenine nucleotide changes in the remnant liver: An early signal for regeneration after partial hepatectomy.

机译：残留肝脏中腺嘌呤核苷酸的变化：部分肝切除术后再生的早期信号。

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摘要

Liver regeneration after partial hepatectomy (PHx) is orchestrated by multiple signals from cytokines and growth factors. We investigated whether increased energy demand on the remnant liver after PHx contributes to regenerative signals. Changes in the tissue's energy state were determined from adenine nucleotide levels. Adenosine triphosphate (ATP) levels in remnant livers decreased markedly and rapidly (to 48% of control by 30 seconds post-PHx) and remained significantly lower than those in sham-operated controls for 24 to 48 hours. The ATP decrease was not reflected in corresponding increases in adenosine diphosphate (ADP) and adenosine monophosphate (AMP), resulting in a marked decline in total adenine nucleotides (TAN). We found no evidence of mitochondrial damage or uncoupling of oxidative phosphorylation. Multiple lines of evidence indicated that the decline in TAN was not caused by increased energy demand, but by ATP release from the liver. The extent of ATP loss was identical after 30% or 70% PHx, whereas fasting or hyperglycemia, conditions that greatly alter energy demand for gluconeogenesis, affected the ATP/ADP decline but not the loss of TAN. Presurgical treatment with the alpha-adrenergic antagonist phentolamine completely prevented loss of TAN, although changes in ATP/ADP were still apparent. Importantly, phentolamine treatment inhibited early signaling events associated with the priming stages of liver regeneration and suppressed the expression of c-fos. Pretreatment with the purinergic receptor antagonist suramin also partly suppressed early regenerative signals and c-fos expression, but without preventing TAN loss. CONCLUSION: The rapid loss of adenine nucleotides after PHx generates early stress signals that contribute to the onset of liver regeneration.
机译：部分肝切除术后的肝再生由细胞因子和生长因子的多种信号共同调控。我们调查了PHx后残余肝脏对能量的需求增加是否有助于再生信号。从腺嘌呤核苷酸水平确定组织能量状态的变化。残余肝脏中的三磷酸腺苷（ATP）水平显着且迅速下降（PHx后30秒降至对照组的48％），并且在24至48小时内仍显着低于假手术对照组。 ATP的降低没有反映在二磷酸腺苷（ADP）和单磷酸腺苷（AMP）的相应增加中，导致总腺嘌呤核苷酸（TAN）显着下降。我们没有发现线粒体损伤或氧化磷酸化解偶联的证据。多条证据表明，TAN下降不是由能量需求增加引起的，而是由肝脏释放的ATP引起的。在30％或70％的PHx后，ATP的损失程度是相同的，而禁食或高血糖（极大地改变糖异生的能量需求的条件）会影响ATP / ADP的下降，但不会影响TAN的损失。尽管ATP / ADP的变化仍然很明显，但使用α-肾上腺素拮抗剂酚妥拉明进行术前治疗可以完全防止TAN的丢失。重要的是，酚妥拉明治疗抑制了与肝脏再生启动阶段有关的早期信号传导事件，并抑制了c-fos的表达。嘌呤能受体拮抗剂苏拉明预处理也可以部分抑制早期再生信号和c-fos表达，但不能防止TAN丢失。结论：PHx后腺嘌呤核苷酸的快速丢失会产生早期应激信号，从而促进肝脏再生。

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