Isoflurane protects renal function against ischemia and reperfusion through inhibition of protein kinases, JNK and ERK
Isoflurane protects renal function against ischemia and reperfusion through inhibition of protein kinases, JNK and ERK
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DOI：
10.1213/01.ane.0000184044.51749.b8
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发表时间：
2005-12-01
影响因子：
5.7
通讯作者：
Sumikawa, K
中科院分区：
文献类型：
--
作者：
Hashiguchi, H;Morooka, H;Sumikawa, K
异氟烷对心脏和大脑的缺血具有药理学预处理作用，但这是否也发生在肾脏中尚不清楚。在这项研究中，我们研究了异氟醚在大鼠肾脏中的药理学预处理。异氟醚预处理组（肾缺血前1.5%异氟烷20分钟）血清肌酐（1.2 +/- 0.7和1.1 +/- 0.2 mg/ dL）和血尿素氮再灌注后24和48 h，缺血再灌注组的血浆中MDA含量分别为99.29和187.31 mg/ dL，显著低于非预处理组（肌酐; 2.4 +/- 1.2和2.9 +/- 0.9 mg/dL，尿素; 62 +/- 19和79 +/- 20 mg/dL）。我们还研究了异氟醚预处理在肾脏中的细胞内信号转导。预处理组大鼠肾脏中JNK和ERK的活性显著低于非预处理组（P < 0.05），而p38活性无显著差异（P> 0.05）。我们的结论是，异氟醚有预处理作用，对肾缺血/再灌注损伤时，缺血前给药。JNK和ERK蛋白激酶的抑制可能参与了异氟醚预处理的机制。
Isoflurane has a pharmacological preconditioning effect against ischemia in the heart and brain, but whether this also occurs in the kidney is unclear. In this study, we investigated pharmacological preconditioning by isoflurane in the rat kidney. In the isoflurane preconditioning group (1.5% isoflurane for 20 min before renal ischemia) serum creatinine (1.2 +/- 0.7 and 1.1 +/- 0.2 mg/ dL) and blood urea nitrogen (99 29 and 187 31 mg/ dL) were significantly smaller at 24 and 48 h after reperfusion than in the nonpreconditioning group (creatinine; 2.4 +/- 1.2 and 2.9 +/- 0.9 mg/dL, urea; 62 +/- 19 and 79 +/- 20 mg/dL). We also investigated the intracellular signal transduction involved in isoflurane preconditioning in the kidney. The activities of the stress protein kinases, JNK and ERK but not p38, were significantly less in the kidneys of the preconditioning group than in those of the nonpreconditioning group (P < 0.05). We conclude that isoflurane has a preconditioning effect against renal ischemia/reperfusion injury when administered before ischemia. Inhibition of the protein kinases, JNK and ERK, might be involved in the mechanisms of isoflurane preconditioning.