Isoflurane protects renal function against ischemia and reperfusion through inhibition of protein kinases, JNK and ERK.

缺血/再灌注损伤（IRI）是外科手术中的主要问题。异氟烷对心脏和大脑中的IR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，我们测试的假设，异氟醚对IRI在大鼠肾脏的保护作用，并进一步JNK抑制有助于这种保护作用。F组仅行假手术。G组在假手术前吸入1.5%异氟醚。H组和I组通过夹闭肾蒂使左肾缺血40分钟。I组在肾缺血前吸入1.5%异氟醚20 min。分别于缺血再灌注0、5、40、90 min和假手术后40 min取肾，检测JNK活性，H组（缺血组）JNK活性在再灌注后5 min即明显激活，40 min达高峰，并维持较高水平至再灌注后90 min。I组（异氟醚）再灌注后40 ~ 90 min JNK活性显著低于H组。我们的结论是，异氟醚有保护作用，对肾IRI时，缺血前给药，该效果将涉及抑制JNK。

Ischemia/reperfusion injury (IRI) is a major problem in the surgery. Isoflurane has a pharmacological preconditioning effect against IR in the heart and brain, but whether this also occurs in the kidney is still unclear. In this study, we tested the hypothesis that isoflurane had a protective effect against IRI in the rat kidney, and further that JNK inhibition contributed this protective effect.Animals were randomly divided into four groups. Group F underwent sham surgery only. Group G received 1.5% isoflurane before sham surgery. Groups H and I were subjected to 40-min left renal ischemia by clamping the renal pedicles. Group I received 1.5% isoflurane for 20 min before renal ischemia. Ischemic kidneys were harvested at 0, 5, 40 and 90 min after starting reperfusion, and sham kidneys were harvested at 40 min after sham surgery, for measurement of JNK activities.JNK was markedly activated as early as 5 min after starting reperfusion, with a peak at 40 min, and remained at a relatively high level until 90 min after starting reperfusion in group H (ischemia only). The activity of JNK in group I (with isoflurane) was significantly lower than in group H from 40 to 90 min after starting reperfusion. We conclude that isoflurane has a protective effect against renal IRI when administered before ischemia and that the effect would involve the inhibition of JNK.