Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany.
Brain Res. 2010 Mar 4;1317:268-76. doi: 10.1016/j.brainres.2009.12.067. Epub 2010 Jan 4.
Edema in the ischemic neural tissue develops by increased vascular permeability associated with extravasation of albumin, and by glial swelling. Here, we show that bovine serum albumin acutely administered to slices of the rat retina causes swelling of glial somata under hypoosmotic conditions. The effect of albumin was dose-dependent, with half-maximal and maximal effects at 10 nM and 1 microM, respectively, and was mediated by activation of transforming growth factor-beta receptor type II, oxidative stress, and the production of arachidonic acid and prostaglandins. Albumin-induced glial swelling was prevented by glutamate and purinergic receptor agonists. The data suggest that serum albumin may induce glial swelling in the presence of osmotic gradients.
缺血性神经组织中的水肿是通过血管通透性增加伴白蛋白渗出以及神经胶质细胞肿胀而发展的。在这里,我们发现牛血清白蛋白在低渗条件下急性给药于大鼠视网膜切片会引起神经胶质细胞体肿胀。白蛋白的作用呈剂量依赖性,半最大和最大效应分别为 10 nM 和 1 μM,并且由转化生长因子-β受体 II 型的激活、氧化应激以及花生四烯酸和前列腺素的产生介导。谷氨酸和嘌呤能受体激动剂可预防白蛋白诱导的神经胶质细胞肿胀。数据表明,在存在渗透梯度的情况下,血清白蛋白可能会诱导神经胶质细胞肿胀。