Functions of Reactive Astrocytes in Ischemic Brain Injury

Abstract

Stroke is the second leading cause of death worldwide. It is important to investigate the pathophysiology of astrocytes, which constitute the most common glial cell group in the mammalian central nervous system (CNS), in the acute and chronic stages of stroke. In pathological conditions following disease and brain damage, astrocytes transform into reactive form. It has been proven by studies that they alleviate oxidative stress damage by releasing GSH (Glutathione) after ischemic injury, contribute to neuron development and survival by secreting neurotrophic factors, have a role in the regulation of cerebral edema, and contribute to angiogenesis by secreting erythropoietin and inhibit neuronal apaptosis. However, besides all these, it has been shown that it causes neuronal death and increases the permeability of the BBB by inducing excitotoxicity after ischemia and causing excessive release of inflammatory factors. There are studies showing that the glial scar formed after ischemic injury provides homeostasis in healthy tissue by preventing the spread of tissue damage in the acute period, but prevents axon growth in the chronic period. Therefore, the functions of reactive astrocytes are controversial. It has been found that genetically reactive astrocytes can undergo transformation into two polarization states, neurotoxic (A1) and neuroprotective (A2). Different types of astrocytes will help discover effective treatment approaches for neurological diseases. In this review; the functions of reactive astrocytes in stroke caused by ischemic brain injury the physiological and histomorphological changes of astrocytes in this process are included.

Keywords

• Stroke
• astrocyte
• blood–brain barrier
• cerebral edema
• oxidative stress.

İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları

Abstract

İnme, dünya çapında ikinci önde gelen ölüm nedenidir. Memeli merkezi sinir sistemindeki (MSS) en yaygın glial hücre grubunu oluşturan astrositlerin inmenin akut ve kronik evresindeki patofizyolojilerinin araştırılması önemlidir. Hastalık ve beyin hasarlarını takiben görülen patolojik durumlarda astrositler reaktif forma dönüşürler. İskemik hasar sonrası Glutatyon (GSH) salgılayarak oksidatif stres hasarını hafiflettikleri, nörotrofik faktörler salgılayarak nöron gelişimi ve sağ kalımına katkıda bulundukları, serebral ödemin düzenlenmesinde rolleri olduğu ve eritropoietin salgılayarak anjiyogeneze katkı sağladığı ve nöronal apoptozu inhibe ettiği yapılan çalışmalarla kanıtlanmıştır. Ancak tüm bunların yanı sıra, iskemi sonrası eksitotoksisiteyi indükleyerek ve inflamatuar faktörlerin aşırı salınımına yol açarak nöronal ölüme yol açtığı ve kan-beyin bariyeri (KBB)’nin geçirgenliğini attırdığı gösterilmiştir. İskemik hasar sonrası oluşan glial skarın akut dönemde doku hasarının yayılmasını önleyerek sağlıklı dokudaki homeostazı sağladığı ancak kronik dönemde akson büyümesine engel olduğunu gösteren çalışmalar mevcuttur. Bu yüzden reaktif astrositlerin işlevleri tartışmalıdır. Genetik olarak reaktif astrositlerin nörotoksik (A1) ve nöroprotektif (A2) iki polarizasyon durumuna dönüşüm geçirebileceği bulunmuştur. Farklı astrosit tipleri nörolojik hastalıklar için etkili tedavi yaklaşımlarının keşfedilmesine yardımcı olacaktır. Bu derlemede; iskemik beyin hasarına bağlı olarak oluşan inmede reaktif astrositlerin fonksiyonlarına ve bu süreçte astrositlerin fizyolojik ve histomorfolojik değişimlerine yer verilmiştir.

Keywords

• İnme
• astrosit
• kan-beyin bariyeri
• serebral ödem
• oksidatif stres.

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