Review Artikel: Target Aksi Obat Antiepilepsi Terhadap Reseptor Kanal Ion Natrium
Abstract
Ion channels are selective pore complexing proteins. One of the ions that can be passed is sodium ion (Na+). Disturbances in the sodium channel (Na+) can be caused epilepsy disease. Epilepsy is a neurological condition characterized by recurrent seizures caused by brief disorders of electrical function in the brain. The purpose of this review is to determine the sodium ion channel receptor as a target for the action of antiepileptic drugs. The method used is based on a literature study. A total of 17 journals through the Google Scholar search engine, PubMed, ScienceDirect, and Microbiology Textbook were applied. The result of analysis using the entire reference showed that the mechanism of action of anti-epileptic drugs is specific for inhibition of the Na+ which is known that depend on the action potential. Examples of drugs are Phenytoin, Carbamazepine, & Lamotrigine. Phenytoin works by binding and blocking active sodium ion channels to reduce the number of open channels along the axon/cell body so that it will inhibit high-frequency release by slowing channel replacement and blocking continuous sodium currents. In addition, Carbamazepine works by blocking Na+ channels, so that there is no influx/entry of Na+ into the nerve cells. It will be effect that excessive depolarization does not occur and seizures can be stopped immediately. Another drug, Lamotrigine is similar to Phenytoin and Carbamazepine. The mechanism is voltage-dependent sodium channel conductance, stabilizing the nerve membrane thereby modulating the release of presynaptic excitatory neurotransmitters and inhibiting presynaptic glutamate.
References
Bagal, S. K., Marron, B. E., Owen, R. M., Storer, R. I., & Swain, N. A. (2015). Voltage gated sodium channels as drug discovery targets. Channels, 9(6), 360–366. https://doi.org/10.1080/19336950.2015.1079674
Chaffey, N. (2003). Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. Molecular biology of the cell. 4th edn.
Colombo, E., Franceschetti, S., Avanzini, G., Mantegazza, M. (2013). Phenytoin Inhibits the Persistent Sodium Current in Neocortical Neurons by Modifying Its Inactivation Properties. PLOS One, 8(1), 1-13.
Fransiska, A. N., Pratama, A. A., Nurayuni, T., Wulanbirru, P., Cordova, D. M., Advaita, C. V.,Mulki, M. A, Malau J. (2022). Jurnal Pendidikan dan Konseling Review : Target Aksi Obat Terhadap Reseptor Dopamin. 4, 8706–8716.
Husna, M., & Kurniawan, S. N. (2018). Biomolecular mechanism of anti epileptic drugs. Malang Neurology Journal, 4(1), 38-45.
Ikawati, Z. (2018). Farmakologi Molekuler: Target Aksi Obat dan Mekanisme Molekulernya. UGM PRESS.
Irawan, D.A.H., Ryandha, M.G., Granadha, S., Windari, W., Abbas Z.A., Rahmawati N.D., Mulki MA., Malau, J. (2022). REVIEW: Mekanisme Molekuler Obat Glibenklamid (Obat Anti Diabetes TIPE-2) Sebagai Target Aksi Obat Kanal Ion Kalium. Jurnal Pendidikan dan Konseling, 9463-9474.
Khairani, A. F., & Sejahtera, D. P. (2019). Strategi pengobatan epilepsi : monoterapi dan politerapi. Universitas Gajah Mada, 18(3), 115–119. https://journal.ugm.ac.id/bns/article/view/55017
Kusumawardhani, R.A., Yuniar, A., Ariyanto, E.J., Maariz, M.F., Tiwi Ambarati T., Anggun, Y., Mulki, M.A.,Malau, J. (2022). Target Aksi Obat Gefatinib Pada Reseptor Tirosin Kinase Terhadap Penyakit Kanker Paru. Jurnal Pendidikan dan Konseling, 9017-9023.
Li, Z. M., Chen, L. X., Hua, L. (2019). Voltage-gated Sodium Channels and Blockers: An Overview and Where Will They Go?. Current Medical Science, 39 (6), 863-873.
Novianae, L., & Sumarno, S. (2020). Ligan SV2A sebagai Terapi Epilepsi. Jurnal Farmasi Udayana, 9(1), 01. https://doi.org/10.24843/jfu.2020.v09.i01.p01
Pathak, S., Waheed, A., & Mirza, R. (2016). Epilepsy: A brief review. PharmaTutor, 4(9), 21-28.
Petty, S. J., Milligan, C. J., Todaro, M., Richards, K. L., Kularathna, P. K., Pagel, C. N., French, C. R., Hill-Yardin, E. L., O’Brien, T. J., Wark, J. D., Mackie, E. J., & Petrou, S. (2016). The antiepileptic medications carbamazepine and phenytoin inhibit native sodium currents in murine osteoblasts. Epilepsia, 57(9), 1398–1405. https://doi.org/10.1111/epi.13474
Qiao, X., Sun, G., Clare, J. J., Werkman, T. R., & Wadman, W. J. (2014). Properties of human brain sodium channel α-subunits expressed in HEK293 cells and their modulation by carbamazepine, phenytoin and lamotrigine. British Journal of Pharmacology, 171(4), 1054–1067. https://doi.org/10.1111/bph.12534
Qiyaam, N., Rahem, A., Maria Pia, D., & Lestiono. (2015). Analisis Efektivitas Biaya (Cost Effectiveness Analysis) Penggunaan Amitryptiline Dibandingkan Carbamazepine pada Pasien Nyeri Neuropatik (Studi Kasus Di Klinik Saraf Rumkital. Dr. Ramelan Surabaya). Jurnal Pharmascience, 2(2), 47–55. http://jps.ppjpu.unlam.ac.id/
Shorvon S. D. (2012). The etiologic classification of epilepsy. Epilepsia, 52(6), 1052–1057.
Sills, G. J. (2012). Mechanisms of action of antiepileptic drugs. Epilepsy, 295-303.
Syafii Harahap, H., Indrayana, Y., & Amalia, E. (2017). Pola Pengobatan dan Fungsi Kognitif Pasien Epilepsi di RSJ Mutiara Sukma. Jurnal Kedokteran Brawijaya, 29(4), 335–340. https://doi.org/10.21776/ub.jkb.2017.029.04.9
Wahyuni, R., Halim, A., & Irawati, Y. S. (2015). Mikroenkapsulasi Karbamazepin Dengan Polimer Hpmc Menggunakan Metoda Emulsifikasi Penguapan Pelarut. Jurnal Farmasi Higea, 7(2), 190–207.
Wibowo, S. (2017). Politerapi dalam Manajemen Epilepsi. Berkala Ilmu Kedokteran, 29(4), 207–212.
Zakiyah, W., Putri, S., Wibowo, S., Elyyana, N., & Nur, S. A. Malau J. (2022). Literature Review : Study of Molecular Mechanism Level of NSAID Class Of Drugs As COX-2 Inhibitors. J Edu healt. 13(02), 572–580.
