Oksidatif stresin endotel disfonksiyon oluşumundaki rolünün araştırılması
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Tarih
2019
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Yayıncı
Hatay Mustafa Kemal Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Endotel, kardiyovasküler sistem içerisinde yer alan, damar iç çeperlerini saran dokudur. Endotel doku, mezoderm kaynaklı tek katlı yassı epitel hücreleri ve bu hücrelerin sentezlediği çeşitli faktörler aracılığıyla vasküler tonusun, hücre adezyonunun, inflamasyonun, damar geçirgenliğinin ve koagülasyonun kontrolünün düzenlenmesinde önemli rol oynamaktadır. Bu fizyolojik ve patolojik olaylardaki herhangi bir dengesizlik endotel disfonksiyona neden olmaktadır. Endotel disfonksiyonu, ateroskleroz, hipertansiyon, diyabet gibi birçok hastalığa neden olabileceği gibi bunların sonucunda da ortaya çıkabilir. Yüksek konsantrasyondaki glukoz hücrede oksidatif stres oluşturmakta, oluşan oksidatif stres hem metabolik hem de aterosklerotik hastalıklarda vasküler hasara yol açan endotel disfonksiyonunun patogenezindeki ana mekanizma olarak kabul edilmektedir. Yapılan bu çalışmada amaç, oksidatif stresin endotel disfonksiyonunda, kilit rol oynayan proteinleri kodlayan genlerin ekspresyon değişimleri üzerindeki etkisini araştırmaktır. Çalışmamızda HUVEC hücreleri 4,5 g/L glukoz içeren (yüksek konsantrasyon glukoz /high glukoz) (HG) çoğaltılarak oksidatif stres modeli oluşturuldu. Kontrol grubu olarak 1 g/L glukoz içeren (Normal konsantrasyon glukoz/normo glukoz) (NG) besiyerinde çoğaltılan hücreler kullanıldı. HG besi yerinde çoğaltılan hücrelerde MDA düzeyi kontrol grubuna göre (NG besiyerinde kullanılan hücre grubu) anlamlı derecede yüksek bulundu (p<0.001). Oksidatif stresin HUVEC hücrelerinde ET1, eNOS ve VCAM genlerinin ekspresyon değişimleri incelendi. Gen ekspresyonları Real Time PCR kullanılarak yapıldı. HG besiyerinde çoğaltılan HUVEC hücrelerinde, VCAM 1 ve eNOS gen ekspresyon düzeylerinde anlamlı bir artış gözlenirken (p <0.05), ET-1 gen ekspresyonunda bir fark gözlenmedi (p> 0.05) . Oksidatif stres, HUVEC hücrelerinde eNOS ve VCAM genlerinin ekspresyon düzeylerini arttırarak endotel disfonksiyonuna neden olmaktadır.
The endothelium is a tissue located in the cardiovascular system that surrounds the inner vascular walls and plays an important role in regulating vascular tone, cell adhesion, inflammation, vascular permeability and coagulation through mesoderm-originated single-layered flat epithelial cells and the various factors synthesized by these cells. Any instability in these physiological and pathological events causes endothelial dysfunction. Endothelial dysfunction may also result in many diseases such as atherosclerosis, hypertension, diabetes, hypercholesterolemia and heart failure, as well as in the result. Oxidative stress, one of the risk factors associated with these developments, atherosclerosis and cardiovascular morbidity and mortality, is thought to facilitate endothelial dysfunction mechanisms. ROS (reactive oxygen species), reactive intermediates for molecular oxygen, have important roles in the cell. However, the imbalance between reactive ROS production and antioxidant defense systems has a primary impetus in the formation of endothelial dysfunction leading to vascular injury in both metabolic and atherosclerotic diseases. That is, increased oxidative stress is regarded as the main mechanism in the pathogenesis of endothelial dysfunction. In our study, oxidative stress model was created by growing HUVEC cells in medium containing 4.5 g/L glucose (high concentration glucose / high glucose) (HG). Cells grown in medium containing 1 g / L glucose (normal concentration glucose / normo glucose) (NG) were used as control group. MDA levels were significantly higher in cells grown in HG medium than in control group (NG medium group) (p <0.001). Expression changes of ET1, eNOS and VCAM1 oxidative stress genes in HUVEC cells were examined. Gene expressions were performed using Real Time PCR. While there was a significant increase in, eNOS VCAM1 gene expression levels in HUVEC cells grown in HG medium (p <0.05), no difference was observed in ET-1 gene expression (p> 0.05). Oxidative stress caused endothelial dysfunction by increasing gene expression of VCAM 1 and eNOS in HUVEC cells.
The endothelium is a tissue located in the cardiovascular system that surrounds the inner vascular walls and plays an important role in regulating vascular tone, cell adhesion, inflammation, vascular permeability and coagulation through mesoderm-originated single-layered flat epithelial cells and the various factors synthesized by these cells. Any instability in these physiological and pathological events causes endothelial dysfunction. Endothelial dysfunction may also result in many diseases such as atherosclerosis, hypertension, diabetes, hypercholesterolemia and heart failure, as well as in the result. Oxidative stress, one of the risk factors associated with these developments, atherosclerosis and cardiovascular morbidity and mortality, is thought to facilitate endothelial dysfunction mechanisms. ROS (reactive oxygen species), reactive intermediates for molecular oxygen, have important roles in the cell. However, the imbalance between reactive ROS production and antioxidant defense systems has a primary impetus in the formation of endothelial dysfunction leading to vascular injury in both metabolic and atherosclerotic diseases. That is, increased oxidative stress is regarded as the main mechanism in the pathogenesis of endothelial dysfunction. In our study, oxidative stress model was created by growing HUVEC cells in medium containing 4.5 g/L glucose (high concentration glucose / high glucose) (HG). Cells grown in medium containing 1 g / L glucose (normal concentration glucose / normo glucose) (NG) were used as control group. MDA levels were significantly higher in cells grown in HG medium than in control group (NG medium group) (p <0.001). Expression changes of ET1, eNOS and VCAM1 oxidative stress genes in HUVEC cells were examined. Gene expressions were performed using Real Time PCR. While there was a significant increase in, eNOS VCAM1 gene expression levels in HUVEC cells grown in HG medium (p <0.05), no difference was observed in ET-1 gene expression (p> 0.05). Oxidative stress caused endothelial dysfunction by increasing gene expression of VCAM 1 and eNOS in HUVEC cells.
Açıklama
Anahtar Kelimeler
Tıbbi Biyoloji, Medical Biology
