ÇAĞRI ÖNER, Hatice İSAN, Ranan Gülhan AKTAŞ, Ertugrul COLAK

Vitamin D’nin Hepatoselü ler Karsinom Ü zerindeki Etkisi

Hepatoselüler karsinoma (HCC) dünya çapında görülme sıklığı açısından en çok görülen dördüncü kanser türüdür. Bu kanser türünün görülme nedenlerinin başında Tip II diyabet, obezite ve alkol kullanımı gelmektedir. Çalışmamızda, karaciğer hastalıklarında etkili olan, ancak hücresel mekanizmalar açısından etkileşimi henüz tam olarak belirlenemeyen vitamin D’nin hem ilaç formu hem de aktif formu olan 1,25-dihidroksivitaminin [1,25(OH)2D3] HepG2 hepatoselüler karsinom hücrelerinin karakteristik özelliklerinde oluşturduğu değişimlerin belirlenmesi amaçlanmıştır. HepG2 hücrelerine vitamin D’nin hem ilaç formu hem de 1,25(OH)2D3 formu ayrı ayrı uygulanarak en etkili konsantrasyonları ve saatleri belirlendi. Bu aşamadan sonra uygun konsantrasyon ve saatte uygulanan her iki maddenin HepG2 hücrelerinin proliferasyonu, adezyonu ve immunohistokimyasal olarak p53 miktarındaki etkileri belirlendi. Elde edilen verilere göre, 250 nM vitamin D’nin ilaç formu HepG2 hücrelerine uygulandıktan 96 saat; 250 nM 1,25(OH)2D3 uygulandıktan sonra 48 saat sonra kontrol grubuna göre istatistiksel olarak proliferasyonun en çok görüldüğü konsantrasyon ve saat olarak belirlendi. Hem vitamin D’nin ilaç hem de 1,25(OH)2D3 formu HepG2 hücrelerinin adezyonunu kontrol grubuna göre istatistiksel olarak anlamlı bir şekilde azaldığı belirlendi (p

The Effect of Vitamin D on Hepatocellülar Carcinoma

Hepatocellular carcinoma (HCC) is the fourth most common cancer in terms of its incidence worldwide. The main causes of this type of cancer are Type II diabetes, obesity and alcohol. In this study, we aimed to determine the changes of both drug form and 1,25-dihydroxyvitamin [1,25(OH)2D3] form of vitamin D which is effective in liver diseases, but the interaction of cellular mechanisms is still unknown, on characteristics of HePG2 hepatocellular carcinoma cells. Both drug and 1,25(OH)2D3 form of vitamin D were applied separately to HepG2 cells and optimal concentrations and hours were determined. Then the proliferation, adhesion and immunohistochemically p53 amount of HepG2 cells were determined by the effects of both substances applied at the optimal concentration and hour. According to our obtained data, the optimal concentration and hour of each vitamin D substances was determined as 96th hour at 250 nM for drug form; 48th hour at 250 nM for 1,25(OH)2D3 form by observing the proliferation rates. It was determined that both drug and 1.25(OH)2D3 forms of vitamin D decreased adhesion of HepG2 cells statistically compared to the control group (p

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