肝脂肪变性可阻止异氟醚诱导大鼠肝脏血红素加氧酶-1的表达。
Hepatic steatosis prevents heme oxygenase-1 induction by isoflurane in the rat liver.
机构信息
Department of Anesthesiology and Critical Care Medicine, Freiburg University Medical Center, D-79106 Freiburg, Germany.
出版信息
World J Gastroenterol. 2011 Oct 7;17(37):4184-90. doi: 10.3748/wjg.v17.i37.4184.
AIM
To characterize the inductive effects of isoflurane (ISO) on hepatic heme oxygenase-1 (HO-1) in an animal model of hepatic steatosis.
METHODS
Lean (LEAN) and obese (FAT) Zucker rats were randomized into 4 groups: 1: LEAN + pentobarbital sodium (PEN); 2: LEAN + ISO; 3: FAT + PEN; 4: FAT + ISO. The animals were mechanically ventilated for 6 h. In vitro analyses of liver tissue included determination of HO-1 mRNA and protein expression as well as measurement of HO enzyme activity and immunohistochemical analyses.
RESULTS
Compared to PEN treatment, ISO administration profoundly induced hepatic HO-1 mRNA and protein expression and significantly increased HO enzyme activity in lean Zucker rats. In contrast, no difference in HO-1 gene expression was observed after ISO or PEN anesthesia in obese Zucker rats.
CONCLUSION
The present study demonstrates that ISO is an inducer of hepatic HO-1 gene expression in non-steatotic organs but failed to upregulate HO-1 in steatotic livers.
目的
在肝脂肪变性动物模型中，研究异氟醚（ISO）对肝血红素加氧酶-1（HO-1）的诱导作用。
方法
选择 lean（LEAN）和肥胖（FAT） Zucker 大鼠，随机分为 4 组：1：LEAN + 戊巴比妥钠（PEN）；2：LEAN + ISO；3：FAT + PEN；4：FAT + ISO。动物进行机械通气 6 h。肝组织的体外分析包括 HO-1 mRNA 和蛋白表达的测定，以及 HO 酶活性和免疫组织化学分析。
结果
与 PEN 处理相比，ISO 给药可显著诱导 lean Zucker 大鼠的肝 HO-1 mRNA 和蛋白表达，并显著增加 HO 酶活性。相反，在肥胖 Zucker 大鼠中，ISO 或 PEN 麻醉后，HO-1 基因表达无差异。
结论
本研究表明，ISO 是非脂肪变性器官中肝 HO-1 基因表达的诱导剂，但不能上调脂肪变性肝脏中的 HO-1。
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