Investigation of the Neuroprotective Impact of Nimodipine on Neuro2a Cells by Means of a Surgery-Like Stress Model

International Journal of Molecular Sciences

Eva Herzfeld¹  Christian Strauss¹  Sebastian Simmermacher¹  Kaya Bork³  R࿍iger Horstkorte³  Faramarz Dehghani²  Christian Scheller¹ 

[1] Department of Neurosurgery, Martin-Luther University of Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Saale), Germany; E-Mails:;Department of Anatomy and Cell Biology, Martin-Luther University of Halle-Wittenberg, Große Steinstraße 52, 06108 Halle (Saale), Germany; E-Mail:;Institute for Physiological Chemistry, Martin-Luther University of Halle-Wittenberg, Hollystr. 1, 06114 Halle (Saale), Germany; E-Mails:

关键词: nimodipine;    neuroprotection;    Neuro2a;    stress;    surgery;   

DOI  :  10.3390/ijms151018453

来源: mdpi

【 摘 要 】

Nimodipine is well characterized for the management of SAH (subarachnoid hemorrhage) and has been shown to promote a better outcome and less DIND (delayed ischemic neurological deficits). In rat experiments, enhanced axonal sprouting and higher survival of motoneurons was demonstrated after cutting or crushing the facial nerve by nimodipine. These results were confirmed in clinical trials following vestibular Schwannoma surgery. The mechanism of the protective competence of nimodipine is unknown. Therefore, in this study, we established an in vitro model to examine the survival of Neuro2a cells after different stress stimuli occurring during surgery with or without nimodipine. Nimodipine significantly decreased ethanol-induced cell death of cells up to approximately 9% in all tested concentrations. Heat-induced cell death was diminished by approximately 2.5% by nimodipine. Cell death induced by mechanical treatment was reduced up to 15% by nimodipine. Our findings indicate that nimodipine rescues Neuro2a cells faintly, but significantly, from ethanol-, heat- and mechanically-induced cell death to different extents in a dosage-dependent manner. This model seems suitable for further investigation of the molecular mechanisms involved in the neuroprotective signal pathways influenced by nimodipine.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.