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急性高血糖会加重大鼠肝缺血/再灌注损伤。

Acute hyperglycemia worsens hepatic ischemia/reperfusion injury in rats.

机构信息

Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, CA 94143-0648, USA.

出版信息

J Gastrointest Surg. 2010 Mar;14(3):528-35. doi: 10.1007/s11605-009-1112-3. Epub 2009 Dec 9.

Abstract

BACKGROUND/AIMS: 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.

METHODS

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.

RESULTS

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).

CONCLUSIONS

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.

摘要

背景/目的:已知急性高血糖会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会加重肝 I/R 引起的损伤并放大炎症反应。

方法

大鼠用腹腔内注射 25%葡萄糖或 0.9%氯化钠(10 ml/kg BW)预处理。随后,大鼠进行部分(70%)肝缺血 45 分钟。再灌注 4 小时后,评估肝损伤、氧化应激、炎症和热休克蛋白表达。

结果

与对照组相比,血糖组丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)血清浓度分别为 7832+/-3374 和 10677+/-4110 U/L,肝损伤增加。高血糖 I/R 与肝硝基酪氨酸浓度升高和中性粒细胞浸润增加有关。I/R 上调了对照组中保护性热休克蛋白 HSP32 和 HSP70,但这种保护机制被高血糖抑制:HSP32 表达从 1.97+/-0.89(对照组)降至 0.46+/-0.13(高血糖),HSP70 表达从 18.99+/-11.55(对照组)降至 3.22+/-0.56(高血糖)(与假手术相比,表达均归一化,均 p<0.05 与对照组 I/R 相比)。

结论

急性高血糖通过放大氧化应激和 I/R 的炎症反应加重肝 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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3108/2820661/cb47aa3e4437/11605_2009_1112_Fig1_HTML.jpg

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