Scaccianoce Sergio, Del Bianco Paola, Pannitteri Gaetano, Passarelli Francesca
Department of Human Physiology and Pharmacology Vittorio Erspamer, University of Rome La Sapienza, Piazzale Aldo Moro, 5, 00185 Rome, Italy.
Brain Res. 2004 Apr 9;1004(1-2):208-11. doi: 10.1016/j.brainres.2004.01.028.
It has been proposed that S100B can be a marker for several pathological conditions including brain traumas, blood-brain barrier disruption, and ischemia. Because the hypothalamo-pituitary-adrenal axis is activated in these conditions, we investigated the role of glucocorticoids in the effects of stress on serum S100B. Restraint stress increased S100B levels in control and in adrenalectomized but not in corticosterone-injected rats. Adrenalectomy did not alter basal S100B. These results indicate a glucocorticoid-independent relationship between stress and S100B.
有人提出，S100B可作为多种病理状况的标志物，包括脑外伤、血脑屏障破坏和局部缺血。由于下丘脑-垂体-肾上腺轴在这些状况下会被激活，我们研究了糖皮质激素在应激对血清S100B影响中的作用。束缚应激使对照组和肾上腺切除大鼠的S100B水平升高，但对注射皮质酮的大鼠没有影响。肾上腺切除术并未改变基础S100B水平。这些结果表明应激与S100B之间存在不依赖糖皮质激素的关系。
