中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (31): 2424-2431.

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

雌激素抑制新生鼠缺氧缺血损伤脑组织脂质过氧化反应

  

  • 收稿日期:2012-07-27 修回日期:2012-10-08 出版日期:2012-11-05 发布日期:2012-11-05

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

Hui Zhu1, Xiao Han2, Dafeng Ji2, Guangming Lv2, Meiyu Xu1   

  1. 1 Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
    2 Department of Human Anatomy, Institute of Neurobiology, Medical School of Nantong University, Jiangsu Key Laboratory of Neuroregeneration, Nantong 226001, Jiangsu Province, China
  • Received:2012-07-27 Revised:2012-10-08 Online:2012-11-05 Published:2012-11-05
  • Contact: Meiyu Xu, Associate professor,Chief physician, Master’s supervisor, Department of Pediatrics, Affiliated Hospital of Nantong University,Nantong 226001, Jiangsu Province, China xumeiyu.nt@hotmail.com
  • About author:Hui Zhu★, Master, Attending physician, Department of Pediatrics, Affiliated Hospital of Nantong University,Nantong 226001, Jiangsu Province, China

Abstract:

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.

Key words: hypoxic-ischemic encephalopathy, hypoxic-ischemic brain damage, estrogen, malondialdehyde;free radical, nitric oxide synthase, lipid peroxidation, neonatal rats, neuroprotection, neural regeneration