Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (9): 924-930.doi: 10.4103/1673-5374.133141

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Chrysophanol attenuates lead exposure-induced injury to hippocampal neurons in neonatal mice

Ji Zhang, Chunlin Yan, Shu Wang, Yong Hou, Guiping Xue, Li Zhang   

  1. Department of Pharmacology, Hebei North University, Zhangjiakou, Hebei Province, China
  • Received:2014-04-25 Online:2014-05-20 Published:2014-05-20
  • Contact: Shu Wang, Department of Pharmacology, Hebei North University, Zhangjiakou 075000, Hebei Province, China, shuwang388@163.com.
  • Supported by:

    This study was financially supported by the Science and Technology Commission Foundation of Zhangjiakou City, No. 1021098D, and the Medical Scientific Research Project of Health Bureau of Hebei Province, No. 20100144, and the Natural Science Foundation of Hebei Province, No. H2012405016, and the Innovative Talents Project of Hebei North University, No. CXRC1325, and the Major Projects of Hebei North University, No. ZD201310.

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Abstract:

Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, chrysophanol (0.1, 1.0, 10.0 mg/kg) was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after chrysophanol treatment. Collectively, these findings indicate that chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.