Acute hyperglycemia worsens hepatic ischemia/reperfusion injury in rats.
Acute hyperglycemia worsens hepatic ischemia/reperfusion injury in rats.
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DOI：
10.1007/s11605-009-1112-3
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发表时间：
2010-03
影响因子：
3.2
通讯作者：
Hirose, Ryutaro
中科院分区：
文献类型：
--
作者：
Behrends, Matthias;Martinez-Palli, Graciela;Niemann, Claus U.;Cohen, Sara;Ramachandran, Rageshree;Hirose, Ryutaro
急性高血糖可加重心肌梗死和中风后的缺血/再灌注(I/R)损伤。我们研究了急性高血糖是否加重了肝脏I/R所致的损伤，并放大了肝脏I/R引起的炎症反应。随后，大鼠进行部分(70%)肝脏缺血45min。再灌流4h后，检测肝脏损伤、氧化应激、炎症反应和热休克蛋白表达。血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)分别为7,832 ± 3,374和10,677 ± 4,110U/L的高血糖组肝损伤明显加重，而对照组分别为3,245 ± 2,009和5,386 ± 3,393U/L(p <； 0.05与对照组相比)。高血糖I/R与肝脏硝基酪氨酸浓度升高和中性粒细胞浸润增加相关。I/R可上调保护性热休克蛋白HSP32和HSP70的表达，但这种保护机制可被高血糖抑制：HSP32的表达从1.97 ± 0.89(对照组)降至0.46 ± 0.13(高血糖)，HSP70的表达从18.99 ± 11.55(对照组)降至3.22 ± 0.56(高血糖)(表达正常化至假手术组，p 和lt； 0.05与对照组I/R相比)。急性高血糖通过放大氧化应激和对I/R的炎症反应而加重肝脏I/R损伤。损伤的增加与保护性热休克蛋白HSP32和HSP70的下调有关。
Acute hyperglycemia is known to worsen ischemia/reperfusion (I/R) injury following myocardial infarction and stroke. We investigated whether acute hyperglycemia worsens injury and amplifies the inflammatory response evoked by hepatic I/R. Rats were pretreated with an intraperitoneal injection of 25% glucose or 0.9% sodium chloride (10 ml/kg BW). Subsequently, rats underwent partial (70%) hepatic ischemia for 45 min. After 4 h of reperfusion, hepatic injury, oxidative stress, inflammation, and heat shock protein expression were assessed. Liver injury was increased in the hyperglycemic group with alanine aminotransferase (ALT) and aspartate aminotransferease (AST) serum concentrations of 7,832 ± 3,374 and 10,677 ± 4,110 U/L compared to 3,245 ± 2,009 and 5,386 ± 3,393 U/L (p < 0.05 vs. control). Hyperglycemic I/R was associated with increased liver nitrotyrosine concentrations and increased neutrophil infiltration. I/R upregulated the protective heat shock proteins HSP32 and HSP70 in control animals, but this protective mechanism was inhibited by hyperglycemia: HSP32 expression decreased from 1.97 ± 0.89 (control) to 0.46 ± 0.13 (hyperglycemia), HSP70 expression decreased from 18.99 ± 11.55 (control) to 3.22 ± 0.56 (hyperglycemia), (expression normalized to sham, both p < 0.05 vs. control I/R). Acute hyperglycemia worsens hepatic I/R injury by amplifying oxidative stress and the inflammatory response to I/R. The increase in injury is associated with a downregulation of the protective heat shock proteins HSP32 and HSP70.
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影响因子：
3
作者：
Iwasaki, Yasumasa;Kambayashi, Machiko;Hashimoto, Kozo
通讯作者：
Hashimoto, Kozo
影响因子：
5.8
作者：
Santoro, MG
通讯作者：
Santoro, MG
影响因子：
3.8
作者：
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通讯作者：
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影响因子：
2.1
作者：
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通讯作者：
Hooper, Philip L.
DOI：
10.1016/j.jtcvs.2005.05.049
发表时间：
2005-10-01
影响因子：
6
作者：
Doenst, T;Wijeysundera, D;Borger, MA
通讯作者：
Borger, MA