首页> 外文期刊>American Journal of Physiology >Effect of heat shock preconditioning on NF-kappaB/I-kappaB pathway during I/R injury of the rat liver.
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Effect of heat shock preconditioning on NF-kappaB/I-kappaB pathway during I/R injury of the rat liver.

机译:热休克预处理对大鼠肝脏I / R损伤期间NF-κB/I-κB通路的影响。

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摘要

Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication after liver surgery. Heat shock (HS) preconditioning is an effective strategy for protecting the liver from I/R injury, but its exact mechanism is still unclear. Because the activation of nuclear factor-kappaB (NF-kappaB) is an important event in the hepatic I/R-induced inflammatory response, the effect of HS preconditioning on the pathway for NF-kappaB activation was investigated. In the control group, NF-kappaB was activated 60 min after reperfusion, but this activation was suppressed in the HS group. Messenger RNA expressions of proinflammatory mediators during reperfusion were also reduced with HS preconditioning. Concomitant with NF-kappaB activation, NF-kappaB inhibitor I-kappaB proteins were degraded in the control group, but this degradation was suppressed in the HS group. This study shows that HS preconditioning protected the liver from I/R injury by suppressing the activation of NF-kappaB and the subsequent expression of proinflammatory mediators through the stabilization of I-kappaB proteins.
机译:肝缺血再灌注(I / R)损伤仍然是肝脏手术后的致命并发症。热休克(HS)预处理是保护肝脏免受I / R损伤的有效策略,但其确切机制仍不清楚。由于核因子-kappaB(NF-kappaB)的激活是肝脏I / R诱导的炎症反应中的重要事件,因此研究了HS预处理对NF-kappaB激活途径的影响。在对照组中,NF-κB在再灌注后60分钟被激活,但是在HS组中这种激活被抑制。 HS预处理还可降低再灌注过程中促炎性介质的Messenger RNA表达。与NF-kappaB激活同时,在对照组中NF-kappaB抑制剂I-kappaB蛋白被降解,但在HS组中这种降解被抑制。这项研究表明,HS预处理可通过抑制NF-κB的激活和随后通过I-κB蛋白的稳定表达促炎介质来保护肝脏免受I / R损伤。

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