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Trans-anethole protects cortical neuronal cells against oxygen–glucose deprivation/reoxygenation

Abstract

Trans-anethole has been studied on pharmacological properties such as anti-inflammation, anti-oxidative stress, antifungal and anticancer. However, to date, the anti-ischemic effects of trans-anethole have not been assessed. Therefore, we investigated the neuroprotection of trans-anethole against oxygen–glucose deprivation/reoxygenation (OGD/R)-induced cortical neuronal cell injury, an in vitro model of ischemia. The abilities of trans-anethole to block excitotoxicity, oxidative stress and mitochondrial dysfunction were evaluated in OGD/R-induced neurons. Trans-anethole significantly ameliorated OGD/R-induced neuronal cell injury by attenuating the intracellular calcium overload via the activation of NMDA receptors. Trans-anethole also inhibited OGD/R-induced reactive oxygen species overproduction, which may be derived from the scavenging activity in peroxyl radicals, assessed in an oxygen radical absorbance capacity assay. Furthermore, trans-anethole was shown to attenuate the depolarization of mitochondrial transmembrane. These results indicated that the neuroprotective effect of trans-anethole on OGD/R-induced neuronal injury might be due to its ability to inhibit excitotoxicity, oxidative stress and mitochondrial dysfunction. Considering these multiple pathways causing ischemic neuronal damage, the multi-functional effect of trans-anethole suggested that it may be effective in treating ischemic stroke.

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Acknowledgments

This research was supported by Grants from the National Research Foundation of Korea (NRF) funded by the Korean government (MEST) (No. 2012R1A2A2A02007145).

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Correspondence to In-Young Choi.

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S. Ryu and G. H. Seol contributed equally to this work.

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Ryu, S., Seol, G.H., Park, H. et al. Trans-anethole protects cortical neuronal cells against oxygen–glucose deprivation/reoxygenation. Neurol Sci 35, 1541–1547 (2014). https://doi.org/10.1007/s10072-014-1791-8

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  • DOI: https://doi.org/10.1007/s10072-014-1791-8

Keywords

  • Trans-anethole
  • Oxygen–glucose deprivation/reoxygenation
  • Neuroprotection
  • Excitotoxicity
  • Oxidative stress