AAS ›› 2014, Vol. 45 ›› Issue (4): 446-451.doi: 10.3969/j.issn.0529-1356.2014.04.002

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Low dose of genistein attenuates neuronal injury and improves learning and memory functions of rats following global cerebral ischemia

MA Wen-dong1 TU Jing-yi2  ZHU Ying1 ZHANG Xi1 TANG Hui1 WANG Rui-min 1*   

  1. 1.Institute of Neurobiology, Medical Experimental and Research Center of Hebei United University, Hebei Tangshan 063000, China; 2. Pathology Staff Room,Tangshan Vocational Technical College, Hebei Tangshan 063000, China)
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  • Received:2013-07-01 Revised:2013-09-06 Online:2014-08-06 Published:2014-08-06
  • Contact: WANG Rui-min E-mail:ruimin-wang@163.com

Abstract:

Objective To explore the neuroprotective role of Genistein (GEN) on hippocampal CA1 neurons and the possible mechanism following global cerebral ischemia (GCI) in rats. Methods Seventy five rats were subjected to global cerebral ischemia (GCI) by four-vessel occlusion and randomly divided into five groups, sham, ischemia/reperfusion (I/R), GEN, ICI 182,780 and vehicle groups. Fluoro-Jade B and neuron-specific nuclear-binding protein (NeuN) staining was used to observe CA1 neuronal survival. TUNEL was used to detect apoptotic neurons. Spatial learning and memory function of the rats were evaluated by Morris water maze. Results The best dose of neuroprotective role of GEN was 1.0mg/kg body weight. Compared with sham, TUNEL-positive neurons in the hippocampal CA1 region increased significantly in I/R and vehicle groups (P<0.01), while posttreatment with GEN (1.0mg/kg) at 5min after ischemia by tail vein injection decreased markedly (P<0.01). Treatment of 1.0mg/kg GEN markedly attenuated spatial learning and memory deficits of the rats after ischemic insult compared to I/R group. Furthermore, ICI 182,780 significantly abolished the neuroprotective role of GEN (P<0.01). Conclusion The low-dose (1.0mg/kg) GEN significantly attenuates neuronal damage and cognitive deficits following GCI in rats, and the mechanism may be involved in estrogen receptor activity.

Key words: Genistein, Ischemia/reperfusion, Hippocampal CA1 region, Estrogen, Terminal UTP nick end labeling, Rat