Production of hydroxyl free radical by brain tissues in hyperglycemic rats subjected to transient forebrain ischemia
Production of hydroxyl free radical by brain tissues in hyperglycemic rats subjected to transient forebrain ischemia
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DOI：
10.1016/s0891-5849(99)00152-5
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发表时间：
1999-11-01
影响因子：
7.4
通讯作者：
Siesjö, BK
中科院分区：
文献类型：
--
作者：
Li, PA;Liu, GJ;Siesjö, BK
已知缺血前高血糖会加重由短暂缺血引起的脑损伤。在这项研究中，我们探讨了这种恶化是否是在早期再灌注期间活性氧（ROS）的形成增强之前。为此，normo和高血糖大鼠进行15分钟的前脑缺血，并允许恢复期为5，15，和60分钟。水杨酸钠腹腔注射剂量为100毫克/公斤，并在再循环过程中进行组织采样，以允许分析水杨酸（SA）及其羟基化产物，2，3-和2，5-二羟基苯甲酸酯（DHBA）。从正常血糖动物的丘脑和尾壳核取样的组织在再循环5和15分钟后未能显示2，3-或2，5-DHBA的增加。然而，再循环60分钟后，在新皮层中观察到这种增加，海马中也有增加。hyperplasia有三个影响。首先，再循环15分钟后，它使丘脑和尾壳核中的2，5-DHBA增加至超过正常血糖值的值。其次，它增加了新皮质中2，5-DHBA和总DHBA的基础值。第三，它增加了海马中2，5-和总DHBA的60分钟值。这些结果提示，至少在一定程度上，高血糖症可能通过增强基础和缺血触发的ROS产生而加重损伤。(C)1999 Elsevier Science Inc.
Preischemic hyperglycemia is known to aggravate brain damage resulting from transient ischemia. In the study, we explored whether this aggravation is preceded by an enhanced formation of reactive oxygen species (ROS) during the early reperfusion period. To that end, normo- and hyperglycemic rats were subjected to 15 min of forebrain ischemia and allowed recovery periods of 5, 15, and 60 min. Sodium salicylate was injected intraperitoneally in a dose of 100 mg/kg, and tissues were sampled during recirculation to allow analyses of salicylic acid (SA) and its hydroxylation products, 2,3- and 2,5-dihydroxybenzoate (DHBA). Tissue sampled from thalamus and caudoputamen in normoglycemic animals failed to show an increase in 2,3- or 2,5-DHBA after 5 and 15 min of recirculation. However, such an increase was observed in the neocortex after 60 min of recirculation, with a suggested increase in the hippocampus as well. Hyperglycemia had three effects. First, it increased 2,5-DHBA in the thalamus and caudoputamen to values exceeding normoglycemic ones after 15 min of recirculation Second, it increased basal values of 2,5- and total DHBA in the neocortex. Third, it increased the 60-min values for 2,5- and total DHBA in the hippocampus. These results hint that, at least in part, hyperglycemia may aggravate damage by enhancing basal- and ischemia-triggered production of ROS. (C) 1999 Elsevier Science Inc.