Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

作     者：Hui Zhu Xiao Han Dafeng Ji Guangming Lv Meiyu Xu 

作者机构：Department of Pediatrics Affiliated Hospital of Nantong University Nantong 226001 Jiangsu Province China Department of Human Anatomy Institute of Neurobiology Medical School of Nantong University Jiangsu Key Laboratory ofNeuroregeneration Nantong 226001 Jiangsu Province China 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2012年第7卷第31期

页      面：2424-2431页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 1002[医学-临床医学] 081704[工学-应用化学] 1001[医学-基础医学(可授医学、理学学位)] 07[理学] 08[工学] 0817[工学-化学工程与技术] 09[农学] 0903[农学-农业资源与环境] 

基　　金：supported by the Project of Nantong Application Plan,No.BK2011055 the Project of Nantong University,No.09Z032 

主　　题：hypoxic ischemic encephalopathy hypoxic ischemic brain damage estrogen malondialdehyde free radical nitric oxide synthase lipid peroxidation neonatal rats neuroprotection neural regeneration 

摘      要：Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.