THE EFFECT OF NIMODIPINE ON CALCIUM INTRACELLULAR AND ROS EXPRESSION IN NEURON CULTURE CELL LINE SH-SY5Y INDUCE CHRONIC HIPERGLYCEMIA
DOI:
https://doi.org/10.29121/granthaalayah.v8.i2.2020.219Keywords:
Nimodipine, Diabetic Neuropathy, Calcium Intracellular, ROS, SH-SY5YAbstract [English]
Introduction: A frequent microvascular complication of diabetes mellitus were peripheral neuropathies with a prevalence of around 30-50%. Generally, oxidative stress is the key to the pathological process that induces damage to peripheral nerves in sensory neurons thereby increasing the production of reactive oxygen species (ROS) and mitochondrial dysfunction which causes deregulation of calcium ion homeostasis and disrupted calcium signaling. Nimodipine is an L-type Ca2+ inhibitor that reactivates the ATPase pathway, has a neuroprotective effect and can improve the regulation of blood and nerve flow in restoring the adrenergic function of the vasa nervorum. Aim: The purpose of this study was to determine the effect of 0.5µm nimodipine on intracellular calcium and ROS expression in SH-SY5Y cell cultures induces chronic hyperglycemia.
Method: Normoglycemic glucose-induced cell culture of neurons 25mM, 50mM hyperglycemia for 6 days and then given nimodipine and without 0.5µM nimodipine.
Results: Based on the results of the One-Way ANOVA test, there was a significant difference (p<0.05) in intracellular calcium expression and ROS in cell cultures exposed to chronic hyperglycemia. Nimodipine 0.5µM significantly reduced intracellular calcium expression but did not reduce ROS expression. The Spearman rank correlation test (r=0.5; p>0.05) given nimodipine 0.5µM therapy found a positive correlation, but not significant.
Conclusion: Based on this study it can be concluded that the administration of 0.5µM nimodipine can reduce intracellular calcium expression but has not been able to reduce ROS expression in 50mM glucose-induced cell cultures.
Downloads
References
Deli,G., Bosnyak E., Pusch E., Komoly S., Feher G. Diabetic neuropathies: Diagnosis and management, Neuroendocrinology, 2013, 98(4), 267–280.
El-Najjar, N., Kulkarni R., Nader N., Hodeify R., Machaca K. Effects of Hyperglycemia on Vascular Smooth Muscle Ca2+ Signaling, BioMed Research International, 2017.
Gripp, K. W., Ennis, S. and Napoli, J. Exome Analysis in Clinical Practice: Expanding the Phenotype of Bartsocas-Papas Syndrome, American Journal of Medical Genetics, Part A, 2013, 1058–1063.
Guerrero-Hernandez, A. and Verkhratsky, A. Calcium signalling in diabetes, Cell Calcium. Elsevier Ltd, 2014, 56(5), 297–301.
Herzfeld, E., Strauss C., Simmermacher S., Bork K., Horstkorte R., Dehghani F., Scheller C. Investigation of the neuroprotective impact of nimodipine on Neuro2a cells by means of a surgery-like stress model, International Journal of Molecular Sciences, 2014, 15(10), 18453–18465.
Kappelle, A. C., Biessels G.J., Buren T.V., Erkelens D.W., De Wildt D.J. Effects of nimodipine on sciatic nerve blood flow and vasa nervorum responsiveness in the diabetic rat, European Journal of Pharmacology, 1993, 250(1), 43–49.
Pak, E. J., Son, G. D. and Yoo, B. S. Cadmium inhibits neurite outgrowth in differentiating human SH-SY5Y neuroblastoma cells, International Journal of Toxicology, 2014, 33(5), 412–418.
Singh, A., Verma, P., Balaji G., Samantary S., Mohanakumar K.P. Nimodipine, an L-type calcium channel blocker attenuates mitochondrial dysfunctions to protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonism in mice, Neurochemistry International. Elsevier Ltd, 2016, 99, 221–232.
Soelistijo, S. A. et al. Konsensus Pengendalian dan Pencegahan Diabetes Melitus Tipe 2 di Indonesia, Perkeni, 2015.
Veves, A. and Malik, R. A. Diabetic Neuropathy Clinical Management. Second edi. Edited by R. A. M. Aristides Veves. Manchester, UK, 2007.
Kawano, T. Current Overview of Diabetic Neuropathy-Mechanisms, Symptoms, Diagnosis and Treatment. 2014, 89-105.
Walton, E. L. Oxidative stress and Diabetes; Glucose response in the ROS. Biomedical Journal. Elsevier Ltd, 2017, 4(5), 241-244.
Downloads
Published
How to Cite
Issue
Section
License
With the licence CC-BY, authors retain the copyright, allowing anyone to download, reuse, re-print, modify, distribute, and/or copy their contribution. The work must be properly attributed to its author.
It is not necessary to ask for further permission from the author or journal board.
This journal provides immediate open access to its content on the principle that making research freely available to the public supports a greater global exchange of knowledge.
