Abstract
Nimodipine is well characterized for the management of aneurysmal subarachnoid hemorrhage and has been shown to promote a better outcome and less delayed ischemic neurological deficits. Animal and clinical trials show neuroprotective efficacy following nerve injuries. We showed a neuroprotective effect on Neuro2a cells. Subsequent microarray analysis revealed—among others—fatty acid 2-hydroxylase (FA2H) upregulated by nimodipine in vitro, which is a component of myelin synthesis. Differentiated Neuro2a cells were analyzed for nimodipine-mediated survival considering stress treatment in comparison to nifedipine-treatment. Cell survival was determined by measurement of LDH activity in the culture medium. Nimodipine decreased surgery-like stress-induced cell death of differentiated Neuro2a cells. Neuro2a cell culture was analyzed for changes in FA2H expression induced by nimodipine or nifedipine in surgery-like stress conditions. We analyzed expression levels of FA2H mRNA and protein by qPCR using fa2h specific primers or a FA2H-specific antibody in nimodipine or nifedipine non- and pre-treated Neuro2a cell culture, respectively. Nimodipine but not nifedipine increases FA2H protein levels and also significantly increases mRNA levels of FA2H in both undifferentiated and differentiated Neuro2a cells. Our findings indicate that higher expression of FA2H induced by nimodipine may cause higher survival of Neuro2a cells stressed with surgery-like stressors.
Highlights
Nimodipine as well as nifedipine are 1,4-dihydropyridine L-type calcium channel antagonists
Our findings indicate that higher expression of fatty acid 2-hydroxylase (FA2H) induced by nimodipine may cause higher survival of Neuro2a cells stressed with surgery-like stressors
We found, according to recent data in undifferentiated Neuro2a cells, that differentiated Neuro2a cells are protected from mechanical, heat and oxidative stress by nimodipine, or at least to a lower extent by nifedipine
Summary
Nimodipine as well as nifedipine are 1,4-dihydropyridine L-type calcium channel antagonists. Laryngeal and maxillofacial surgery in animal experiments [7,8,9,10], and clinical series it shows a beneficial effect [11,12,13,14,15,16] These results were linked to neuroprotection described by Nuglisch et al [17]. 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 [20]. These represent stressors, which may occur during surgery as described before [20]. We analyzed FA2H mRNA levels regulation in dependence on nimodipine but not on nifedipine
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.