Rewal Mridula, Wen Yi, Simpkins James W, Jung Marianna E
Department of Pharmacology and Neuroscience, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA.
Neurosci Lett. 2005 Mar 22;377(1):44-8. doi: 10.1016/j.neulet.2004.11.067. Epub 2004 Dec 21.
Parvalbumin (PA) is a calcium-binding protein that has been implicated in neuroprotection. We examined whether the stimulus effect of ethanol withdrawal (EW) alters the expression of PA in a manner that is prevented by 17beta-estradiol (E2). Ovariectomized rats implanted with E2 (EW/E2) or oil (EW/Oil) pellets received chronic ethanol (7.5%, w/v, 5 weeks) or control dextrin diets (Dex/Oil). At 24h of EW, rats were tested for overt EW signs, and the cerebellum was prepared for immunoblotting and immunohistological assessment for PA. The EW/Oil group showed a higher EW sign score, a lower PA expression, and fewer PA-positive Purkinje neurons than the dextrin control group. In the EW/E2 group, EW sign scores, PA expression, and PA-positive Purkinje neurons were not significantly different from those in the control dextrin group. These data suggest that E2 treatment protects against the PA-suppression associated with EW toxicity.
小清蛋白（PA）是一种钙结合蛋白，与神经保护作用有关。我们研究了乙醇戒断（EW）的刺激效应是否会以一种可被17β-雌二醇（E2）阻止的方式改变PA的表达。植入E2（EW/E2）或油（EW/Oil）微丸的去卵巢大鼠接受慢性乙醇（7.5%，w/v，5周）或对照糊精饮食（Dex/Oil）。在EW 24小时时，对大鼠进行明显EW体征测试，并制备小脑用于PA的免疫印迹和免疫组织学评估。与糊精对照组相比，EW/Oil组显示出更高的EW体征评分、更低的PA表达以及更少的PA阳性浦肯野神经元。在EW/E2组中，EW体征评分、PA表达和PA阳性浦肯野神经元与对照糊精组无显著差异。这些数据表明，E2治疗可预防与EW毒性相关的PA抑制。
