TY  - JOUR
T1  - Effects of Short-term High Glucose on NIH/3T3 Fibroblast Proliferation, Apoptosis, and Collagen Type I Production
TT  - Kısa Süreli Yüksek Glikoz Uygulamasının NIH/3T3 Fibroblastlarında Proliferasyon, Apoptoz ve Kollajen Tip I Üretimi Üzerine Etkileri
AU  - Kanıgür Sultuybek, Gönül
AU  - Soydaş, Tuğba
AU  - Yaprak Saraç, Elif
AU  - Çınar, Suzan
AU  - Yenmiş, Güven
AU  - Doğan, Sibel
AU  - Solakoğlu, Seyhun
AU  - Tunçdemir, Matem
PY  - 2019
DA  - August
Y2  - 2019
JF  - Tıp Fakültesi Klinikleri Dergisi
JO  - TFK
PB  - İstanbul Aydın Üniversitesi
WT  - DergiPark
SN  - 2630-5585
SP  - 91
EP  - 95
VL  - 2
IS  - 3
LA  - en
AB  - Objective: To investigate the mechanisms of in vitro high glucose induced model of liverfibrosis.Material and methods: The effects of high glucose concentration on fibroblast proliferationwere investigated by BrdU immunostaining. Apoptosis and necrosis levels were analyzed byflow cytometric assay. The content of collagen type I was measured by Collagen EstimationAssay through ELISA.Results: A high glucose medium not only increased NIH/3T3 fibroblast proliferation, but alsoincreased type I collagen synthesis, showing a similar condition to the fibrosis. Moreover, thehigh glucose caused an increased level of cellular apoptosis and necrosis.Conclusions: High glucose modulates the fibrosis in NIH/3T3 fibroblast cells via inducing theproduction of type I collagen while maintains the homeostasis by inducing the apoptosis andnecrosis of cells.
KW  - High glucose
KW  - Collagen
KW  - NIH/3T3 fibroblast
KW  - Apoptosis
N2  - Amaç: Yüksek glikoza bağlı karaciğer fibrozis mekanizmalarını in vitro model kullanarakaraştırmak amaçlanmıştır.Gereç ve yöntem: Yüksek glikoz konsantrasyonunun fibroblast proliferasyonu üzerindekietkileri BrdU immünositokimya tekniği ile incelenmiştir. Apoptoz seviyeleri ve nekroz akımsitometri analizi ile tespit edildi. Kollajen tip I içeriği, ELISA ile ölçüldü.Bulgular: Yüksek glikoz düzeyi sadece NIH/3T3 fibroblast proliferasyonunu arttırmadı, aynızamanda fibrozise benzer bir durumun göstergesi olarak tip I kollajen sentezini de arttırdı.Ayrıca yüksek glikoz, apoptoz ve nekroz seviyelerinin artmasına da neden olmuştur.Sonuç: Yüksek glikoz, NIH/3T3 fibroblast hücrelerinde fibrozisi, tip I kollajen üretiminiindükleyerek modüle ederken, hücrelerin apoptoz ve nekrozunu indükleyerek homeostazı korur.
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UR  - https://dergipark.org.tr/tr/pub/atk/issue//604775
L1  - https://dergipark.org.tr/tr/download/article-file/783751
ER  -