Avunduk Mustafa Cihat, Yurdakul Talat, Erdemli Esra, Yavuz Ayşe
Pathology Department, Selçuk University Faculty of Medicine, 42080 Akyokuş, Konya, Turkey.
Urol Res. 2003 Aug;31(4):280-5. doi: 10.1007/s00240-003-0329-y. Epub 2003 Jul 3.
Ischemia-reperfusion injury in rat kidneys most probably comes from oxidative stress, but the possible preventive effect of alpha-tocopherol (AT) treatment on this injury has not yet been established. Forty male Wistar rats were randomly divided into four groups. The left renal arteries of all rats except the controls were clamped to induce renal ischemia. The left kidneys of the rats in the ischemia group were removed following 40 min ischemia. The rats in the ischemia-reperfusion and ischemia-reperfusion-AT groups were treated similarly, but in these groups the renal arteries were re-perfused for 1 h following ischemia. The rats in the ischemia-reperfusion-AT group also received 10 mg/kg AT 3 h prior to ischemia. The specimens were examined histopathologically and ultrastructurally, and the tissue calcium levels were measured. Light microscope and ultrastructural examination showed that the greatest damage occurred in the ischemia-reperfusion group. The highest level of tissue calcium was also found in this group. In the ischemia-reperfusion-AT-treated group, less tissue damage and a lower tissue calcium concentration was found compared to both the ischemia and ischemia-reperfusion groups. Our results indicate that AT can reduce tissue damage after ischemia-reperfusion injury.
大鼠肾脏的缺血再灌注损伤很可能源于氧化应激,但α-生育酚(AT)治疗对这种损伤的潜在预防作用尚未得到证实。40只雄性Wistar大鼠被随机分为四组。除对照组外,所有大鼠的左肾动脉均被夹闭以诱导肾脏缺血。缺血组大鼠在缺血40分钟后切除左肾。缺血再灌注组和缺血再灌注-AT组的大鼠处理方式类似,但在这些组中,缺血后肾动脉再灌注1小时。缺血再灌注-AT组的大鼠在缺血前3小时还接受了10mg/kg的AT。对标本进行了组织病理学和超微结构检查,并测量了组织钙水平。光镜和超微结构检查显示,缺血再灌注组损伤最严重。该组的组织钙水平也最高。与缺血组和缺血再灌注组相比,缺血再灌注-AT治疗组的组织损伤较轻,组织钙浓度较低。我们的结果表明,AT可以减轻缺血再灌注损伤后的组织损伤。