Galangin Protects AML-12 Cells Against Dactinomycin Induced Hepatotoxicity
Küçük Resim Yok
Tarih
2023
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Galenos Publ House
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Aim: The purpose of this study was to evaluate the effects of galangin (Gal) on dactinomycin induced hepatotoxicity in vitro. Materials and Methods: AML -12 cell line was divided into 4 groups as the control, Gal, dactinomycin, and Gal+dactinomycin groups. IC50 dose was determined by the thiazolyl blue tetrazolium bromide test. Gene expressions of glutathione (GSH), superoxide dismutase (SOD), catalase, caspase 3 (Cas-3), Cas-9, apoptotic protease activating factor -1 (Apaf-1), B cell CLL/lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), tumor protein p53 (p53), second mitochondria -derived activator of caspase/direct inhibitor of apoptosis-binding protein (smac/DIABLO), topoisomerase (Top) I, and Top II were determined with quantitative real-time polymerase chain reaction analysis. Results: Dactinomycin elevated the expression of SOD, catalase, and GSH in response to oxidative effects. In the Gal+dactinomycin group, Gal administration reduced Apaf-1 expression and increased Bcl-2 expression with antiapoptotic effects. In the dactinomycin group, p53 levels increased due to the defense mechanism against DNA damage. Gal increased smac/DIABLO expression to remove damaged structures. Bcl-2 and smac/DIABLO expression levels in the groups were inversely proportional. In the Gal+dactinomycin group, Top II expression level was lower than in the dactinomycin group. This result indicated that double strand of DNA damage was diminished by Gal. Conclusion: Gal protected against the hepatotoxicity due to dactinomycin with antioxidant and antiapoptotic effects. Further experimental studies are needed to establish the use of Gal in liver damage.
Açıklama
Anahtar Kelimeler
Dactinomycin, Galangin, AML-12 Cell Line, Hepatotoxicity, Oxidative Stress, Apoptosis, Hepatopathy-Thrombocytopenia Syndrome, Hepatocellular-Carcinoma, Apoptosis, Mechanisms
Kaynak
Namik Kemal Medical Journal
WoS Q Değeri
N/A
Scopus Q Değeri
Cilt
11
Sayı
3
