Shimizu Shogo, Saito Motoaki, Kinoshita Yukako, Shomori Kohei, Satoh Itaru, Satoh Keisuke
Division of Molecular Pharmacology, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine, Yonago City, Tottori, Japan.
J Urol. 2009 Oct;182(4):1637-43. doi: 10.1016/j.juro.2009.06.010. Epub 2009 Aug 15.
The main pathophysiology of torsion-detorsion is associated with ischemia-reperfusion injury in the testis caused by the twisted spermatic cord and its release. It is most likely mediated by oxygen free radicals. We investigated the effects of ischemic preconditioning and post-conditioning on rat testicular ischemia-reperfusion injury.
Eight-week-old male Sprague-Dawley rats (SLC, Shizuoka, Japan) were randomly divided into 4 age matched groups, including 1-control sham operation, 2-60-minute ischemia/120-minute reperfusion, 3-3 cycles of 5-minute ischemia/5-minute reperfusion and then 60-minute ischemia/120-minute reperfusion (ischemic preconditioning) and 4-60-minute ischemia, 5 cycles of 10-second reperfusion/10-second ischemia and then 120-minute reperfusion (ischemic post-conditioning). After sacrifice the levels of malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, superoxide dismutase, catalase, heat shock protein 70 protein and mRNA, and DNA fragmentation were measured in the rat testes. Testicular tissue was also histologically analyzed.
The levels of malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, heat shock protein 70 mRNA, superoxide dismutase, catalase, DNA fragmentation and apoptosis cells were significantly higher in the ischemia-reperfusion group than in controls. Ischemic preconditioning decreased histological parameters, including vacuolation and necrosis, and decreased malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, heat shock protein 70 mRNA but not protein, superoxide dismutase, catalase, DNA fragmentation and apoptosis compared to the ischemia-reperfusion group. Ischemic post-conditioning ameliorated 8-hydroxydeoxyguanosine, superoxide dismutase, heat shock protein 70 mRNA, DNA fragmentation and apoptosis compared to the ischemia-reperfusion group.
Our data indicate that ischemic preconditioning and post-conditioning ameliorated the testicular damage induced by ischemia-reperfusion injury.
扭转-复位的主要病理生理学与扭转的精索及其松解导致的睾丸缺血-再灌注损伤相关。其很可能由氧自由基介导。我们研究了缺血预处理和后处理对大鼠睾丸缺血-再灌注损伤的影响。
将8周龄雄性Sprague-Dawley大鼠（日本静冈SLC公司）随机分为4个年龄匹配组，包括1-对照假手术组、2-60分钟缺血/120分钟再灌注组、3-3个5分钟缺血/5分钟再灌注周期然后60分钟缺血/120分钟再灌注组（缺血预处理组）和4-60分钟缺血、5个10秒再灌注/10秒缺血周期然后120分钟再灌注组（缺血后处理组）。处死大鼠后，检测大鼠睾丸中丙二醛、8-羟基脱氧鸟苷、髓过氧化物酶、超氧化物歧化酶、过氧化氢酶、热休克蛋白70蛋白和mRNA水平以及DNA片段化情况。对睾丸组织也进行了组织学分析。
缺血-再灌注组丙二醛、8-羟基脱氧鸟苷、髓过氧化物酶、热休克蛋白70 mRNA、超氧化物歧化酶、过氧化氢酶、DNA片段化和凋亡细胞水平显著高于对照组。与缺血-再灌注组相比，缺血预处理降低了包括空泡形成和坏死在内的组织学参数，降低了丙二醛、8-羟基脱氧鸟苷、髓过氧化物酶、热休克蛋白70 mRNA但未降低其蛋白水平、超氧化物歧化酶、过氧化氢酶、DNA片段化和凋亡水平。与缺血-再灌注组相比，缺血后处理改善了8-羟基脱氧鸟苷、超氧化物歧化酶、热休克蛋白70 mRNA、DNA片段化和凋亡情况。
我们的数据表明，缺血预处理和后处理改善了缺血-再灌注损伤诱导的睾丸损伤。
