Induction of heat-shock gene expression in postischemic pig liver depends on superoxide generation.
Induction of heat-shock gene expression in postischemic pig liver depends on superoxide generation.
复制标题
缺血后猪肝中热休克基因表达的诱导取决于超氧化物的产生。
DOI：
10.1016/s0016-5085(94)95209-4
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发表时间：
1994
期刊：
影响因子：
29.4
通讯作者：
Buchman,TG
中科院分区：
文献类型：
--
作者：
Schoeniger,LO;Andreoni,KA;Ott,GR;Risby,TH;Bulkley,GB;Udelsman,R;Burdick,JF;Buchman,TG
出血性休克和心源性休克与复苏时肝休克基因表达有关。本研究探讨了潜在的作用，血管内超氧阴离子作为近端触发热休克蛋白基因expression. Methodspreanesthesized猪进行了120米的总热肝缺血。存活模型包括热的、全肝缺血和再灌注（具有主动门体分流），随后再灌注和存活3天。通过北方和Western分析以及原位RNA杂交来评估系列肝活检样品中热休克蛋白72（HSP-72）信使RNA（mRNA）的表达。血管内O2-作为介质的热休克反应的可能作用进行了评估，其特异性抑制重组人超氧化物歧化酶（SOD）的静脉输注。ResultsIschemia 120分钟，然后再灌注60分钟造成HSP-72 mRNA的积累。转录本定位于肝细胞。HSP-72 mRNA在单纯缺血和再灌注15分钟时均未检测到。三天后，成绩单是不可检测的，但HSP-72蛋白积累的SOD administration.ConclusionsWarm肝缺血诱导HSP-72在再灌注的肝细胞表达的机制，是依赖于超氧阴离子，可能产生intravascularly。然而，超氧化物的瞬时歧化不足以抑制HSP-72随后的积累。
Background/AimsBoth hemorrhagic and cardiogenic shock are associated with hepatic shock gene expression at resuscitation. This study investigated the potential role of intravascular superoxide anion as a proximal trigger of heat shock protein gene expression.MethodsPreanesthetized pigs were subjected to 120 m of total warm hepatic ischemia. The survival model consisted of warm, total hepatic ischemia and reperfusion (with active portal-systemic bypass) followed by reperfusion and survival for 3 days. Serial hepatic biopsy samples were evaluated for the expression of heat shock protein 72 (HSP-72) messenger RNA (mRNA) by Northern and Western analysis and by in situ RNA hybridization. The possible role of intravascular O2−as a mediator of heat shock response was evaluated by its specific inhibition by the intravenous infusion of recombinant human superoxide dismutase (SOD).ResultsIschemia for 120 minutes followed by 60 minutes of reperfusion caused accumulation of HSP-72 mRNA. Transcripts were localized to hepatocytes. HSP-72 mRNA was detected neither following ischemia alone nor when SOD was infused for 15 minutes at reperfusion. Three days later, transcripts were not detectable, but HSP-72 protein accumulated irrespective of SOD administration.ConclusionsWarm hepatic ischemia induces the hepatocyte expression of HSP-72 at reperfusion by a mechanism that is dependent upon the superoxide anion, probably generated intravascularly. However, the transient dismutation of superoxide is insufficient to suppress subsequent accumulation of HSP-72.