Artikel
Nimodipine but not Nifedipine promotes expression of Fatty Acid 2-Hydroxylase in a Surgical Stress Model based on Neuro2a cells
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Autoren
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Eva Herzfeld
- Martin-Luther-Universität Halle-Wittenberg, Medizinische Fakultät, UKH, Klinik für Neurochirurgie, Halle (Saale), Deutschland
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Lea Speh
- Martin-Luther-Universität Halle-Wittenberg, Medizinische Fakultät, UKH, Klinik für Neurochirurgie, Halle (Saale), Deutschland
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Christian Strauss
- Universitätsklinikum Halle/Saale, Klinik und Poliklinik für Neurochirurgie, Halle/Saale, Deutschland
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Christian Scheller
- Neurochirurgie, Halle, Deutschland
| Veröffentlicht: | 9. Juni 2017 |
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Gliederung
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Objective: Nimodipine is recommended for the management of aneurysmal subarachnoid hemorrhage and reduces poor outcomes and delayed ischemic neurological deficits. In skull base, laryngeal and maxillofacial surgery and basic research it shows a beneficial effect for cranial nerve preservation and regeneration. Nifedipine is used in the treatment of hypertension, the vasospastic form of angina pectoris, Raynaud`s disease, and premature labor. Neuroprotection by nimodipine but not by nifedipine was shown in NGF-differentiated PC12 neuronal cells . We showed, that the survival of Neuro2a cells was significantly higher when cells were pre-treated with nimodipine prior to oxidative, mechanical and heat-induced stress. (Differentiated) Neuro2a cells were analysed for nimodipine-mediated survival considering stress treatment in comparison to nifedipine-treatment. Neuro2a cell culture was analysed for changes in fa2h expression,which is a component of myelin synthesis, induced by nimodipine or nifedipine in surgery-like stress conditions.
Methods: Cell survival after stress treatment following nimodipine or nifedipine non- and pre-treatment, respectively, was determined by measurement of LDH activity in the culture supernatant. We analysed expression levels of fa2h by qPCR using fa2h specific primers in nimodipine or nifedipine non- and pre-treated Neuro2a cell culture, respectively.
Results: Nimodipine decreased surgery-like stress-induced cell death of Neuro2a cells. This was not observed for nifedipine. Nifedipine itself rather induces cells death of Neuro2a cells in a dosage dependent manner. Nimodipine but not nifedipine significantly increases mRNA levels of fa2h in both undifferentiated and differentiated Neuro2a cells.
Conclusion: The lethal effect on Neuro2a cells consists with findings, that a neuroprotective effect of nifedipine could not be shown. In contrast to that, the clinically observed neuroprotective effect of nimodipine was verified in our surgery-like stress model. Our findings in qPCR indicate that higher expression of fa2h induced by nimodipine may cause higher survival of Neuro2a cells stressed with surgery-like stressors. This could be possibly linked with higher (re-) myelination of nerve tissue after surgery.
