Neurological Sciences

, Volume 34, Issue 12, pp 2137–2143

Neuroprotective profile of pyruvate against ethanol-induced neurodegeneration in developing mice brain

Authors

  • Najeeb Ullah
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
    • Institute of Basic Medical SciencesKhyber Medical University
  • Muhammad Imran Naseer
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
    • Center of Excellence in Genomic Medicine and Research (CEGMR)King Abdulaziz University
  • Ikram Ullah
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
  • Tae Hyun Kim
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
  • Hae Young Lee
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
    • Division of Life Science, College of Natural Sciences (RINS) and Applied Life ScienceGyeongsang National University
Original Article

DOI: 10.1007/s10072-013-1350-8

Cite this article as:
Ullah, N., Naseer, M.I., Ullah, I. et al. Neurol Sci (2013) 34: 2137. doi:10.1007/s10072-013-1350-8

Abstract

Exposure to ethanol during developmental stages leads to several types of neurological disorders. Apoptotic neurodegeneration due to ethanol exposure is a main feature in alcoholism. Exposure of developing animals to alcohol induces apoptotic neuronal death and causes fetal alcohol syndrome. In the present study, we observed the possible protective effect of pyruvate against ethanol-induced neurodegeneration. Exposure of developing mice to ethanol (2.5 g/kg) induces apoptotic neurodegeneration and widespread neuronal cell death in the cortex and thalamus. Co-treatment of pyruvate (500 mg/kg) protects neuronal cell against ethanol by the reduced expression of caspase-3 in these brain regions. Immunohistochemical analysis and TUNNEL at 24 h showed that apoptotic cell death induced by ethanol in the cortex and thalamus is reduced by pyruvate. Histomorphological analysis at 24 h with cresyl violet staining also proved that pyruvate reduced the number of neuronal cell loss in the cortex and thalamus. The results showed that ethanol increased the expression of caspase-3 and thus induced apoptotic neurodegeneration in the developing mice cortex and thalamus, while co-treatment of pyruvate inhibits the induction of caspase-3 and reduced the cell death in these brain regions. These findings, therefore, showed that treatment of pyruvate inhibits ethanol-induced neuronal cell loss in the postnatal seven (P7) developing mice brain and may appear as a safe neuroprotectant for treating neurodegenerative disorders in newborns and infants.

Keywords

AntioxidantEthanolFetal alcohol syndromeNeurodegenerationNeuroprotectionPyruvate

Copyright information

© Springer-Verlag Italia 2013