Peran Eritropoietin pada Stroke Iskemik Akut

Lisda Amalia, Gilang Nispu Saputra

Abstract


Stroke iskemik merupakan salah satu penyebab stroke tersering, disebabkan oleh oklusi pembuluh darah serebral dan penyebab kematian ketiga. Iskemik otak akan menghasilkan penghasilan mediator inflamasi yang dapat berpartisipasi dalam jejas iskemik di otak. Saat awitan stroke iskemik terjadi, area otak yang diperdarahi oleh pembuluh darah akan kekurangan oksigen dan nutrisi sehingga sel otak terutama neuron berada dalam risiko, neuron ini masih dapat berfungsi yang dikenal sebagai penumbra. Hipoksia jaringan dan iskemik serebral mengaktivasi HIF-1α, yang kemudian mengaktivasi transkripsi gen eritropoietin (EPO) dan Vascular Endothelial Growth Factor (VEGF). Eritropoietin (EPO) merupakan peptida yang juga memiliki efek non–hematopoiesis yaitu berperan mendorong neuroproteksi. Eritropoietin (EPO)  dikeluarkan dalam hitungan menit dari proses iskemik dan mencapai puncak dalam 24 jam dari awitan stroke iskemik. Efek neuroproteksi dari  EPO yaitu sebagai anti apoptosis, anti oksidan, anti inflamasi, anti eksitoksisitas, neurogenesis, angiogenesis dan neurotropik. Dengan kata lain bahwa EPO dapat mengurangi derajat keparahan akibat oklusi pembuluh darah otak.

 

Role of Eritropoietin in Acute Ischemic Stroke

Abstract

Ischemic stroke is one of the most common causes of stroke, caused by cerebral vascular occlusion and the third cause of death. . Ischemic brain will generate income of inflammatory mediators who can participate in ischemic lesions in the brain. When the recitation of an ischemic stroke occurs, areas of the brain that are obscurated by blood vessels will lack oxygen and nutrients so that brain cells, especially neurons, are at risk, these neurons can still function known as penumbra. Tissue hypoxia and cerebral ischemic activate HIF-1α, which then activates the transcription of the Eritropietin (EPO) and Vascular Endothelial Growth Factor (VEGF) genes. Eritropoietin (EPO) is a peptide that also has the effect of non-hematopoiesis which is responsible for encouraging neuroprotection. Eritropietin (EPO) is issued in minutes of an ischemic process and reaches its peak within 24 hours of the onset ischemic stroke. The neuroprotection effect of EPO is as anti-apoptosis, anti-oxidant, anti-inflammatory, anti-excitation, neurogenesis, angiogenesis and neurotropic. In other words, EPO can reduce the severity due to occlusion of brain blood vessels.


Keywords


eritropoietin; neuroproteksi; stroke iskemik; eritropietin; ischemic stroke;, neuroprotection

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DOI: https://doi.org/10.24244/jni.v9i2.262

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