Open Access

Intermittent fasting increases SOD2 and catalase immunoreactivities in the hippocampus but does not protect from neuronal death following transient ischemia in gerbils

  • Authors:
    • Ji Hyeon Ahn
    • Yoohun Noh
    • Bich Na Shin
    • Sung‑Su Kim
    • Joon Ha Park
    • Tae‑Kyeong Lee
    • Minah Song
    • Hyunjung Kim
    • Jae‑Chul Lee
    • Jun‑Hwan Yong
    • Il Jun Kang
    • Yun Lyul Lee
    • Moo‑Ho Won
    • Jong Dai Kim
  • View Affiliations

  • Published online on: September 21, 2018     https://doi.org/10.3892/mmr.2018.9503
  • Copyright: © Ahn et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Intermittent fasting has been shown to have neuroprotective effects against transient focal cerebral ischemic insults. However, the effects of intermittent fasting on transient global ischemic insult has not been studied much yet. The present study examined effects of intermittent fasting on endogenous antioxidant enzyme expression levels in the hippocampus and investigated whether the fasting protects neurons 5 days after 5 min of transient global cerebral ischemia. Gerbils were randomly subjected to either ad libitum or alternate‑day intermittent fasting for two months and assigned to sham surgery or transient ischemia. Changes of antioxidant enzymes were examined using immunohistochemistry for cytoplasmic superoxide dismutase 1 (SOD1), mitochondrial (SOD2), catalase (CAT), and glutathione peroxidase (GPX). The effects of intermittent fasting on ischemia‑induced antioxidant changes, neuronal damage/degeneration and glial activation were examined. The weight of fasting gerbils was not different from that of control gerbils. In controls, SOD1 and GPX immunoreactivities were strong in pyramidal neurons of filed cornu ammonis 1 (CA1). Transient ischemia in controls significantly decreased expressions of SOD1 and GPX in CA1 pyramidal neurons. Intermittent fasting resulted in increased expressions of SOD2 and CAT, not of SOD1 and GPX, in CA1 pyramidal neurons. Nevertheless, CA1 pyramidal neurons were not protected in gerbils subjected to fasting after transient ischemia, and inhibition of glial‑cell activation was not observed in the gerbils. In summary, intermittent fasting for two months increased SOD2 and CAT immunoreactivities in hippocampal CA1 pyramidal neurons. However, fasting did not protect the CA1 pyramidal neurons from transient cerebral ischemia. The results of the present study indicate that intermittent fasting may increase certain antioxidants, but not protect neurons from transient global ischemic insult.

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APA
Ahn, J.H., Noh, Y., Shin, B.N., Kim, S., Park, J.H., Lee, T. ... Kim, J.D. (1899). Intermittent fasting increases SOD2 and catalase immunoreactivities in the hippocampus but does not protect from neuronal death following transient ischemia in gerbils. Molecular Medicine Reports, 0, 0-0. https://doi.org/10.3892/mmr.2018.9503
MLA
Ahn, J. H., Noh, Y., Shin, B. N., Kim, S., Park, J. H., Lee, T., Song, M., Kim, H., Lee, J., Yong, J., Kang, I. J., Lee, Y. L., Won, M., Kim, J. D."Intermittent fasting increases SOD2 and catalase immunoreactivities in the hippocampus but does not protect from neuronal death following transient ischemia in gerbils". Molecular Medicine Reports 0.0 (1899): 0-0.
Chicago
Ahn, J. H., Noh, Y., Shin, B. N., Kim, S., Park, J. H., Lee, T., Song, M., Kim, H., Lee, J., Yong, J., Kang, I. J., Lee, Y. L., Won, M., Kim, J. D."Intermittent fasting increases SOD2 and catalase immunoreactivities in the hippocampus but does not protect from neuronal death following transient ischemia in gerbils". Molecular Medicine Reports 0, no. 0 (1899): 0-0. https://doi.org/10.3892/mmr.2018.9503