Fatty liver mediated by peroxisome proliferator-activated receptor-α DNA methylation can be reversed by a methylation inhibitor and curcumin
Autor: | Jie Cao, Yu Qiang Nie, Dan Tang, Yu Yuan Li, Yong Jian Zhou, Yanlei Du, Chuang Yu Cao |
---|---|
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
chemistry.chemical_classification business.industry Fatty liver Gastroenterology Peroxisome proliferator-activated receptor Methylation medicine.disease Molecular biology 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure chemistry CpG site In vivo Hepatocyte DNA methylation medicine Curcumin 030211 gastroenterology & hepatology business |
Zdroj: | Journal of Digestive Diseases. 19:421-430 |
ISSN: | 1751-2972 |
Popis: | OBJECTIVE Our studies in vitro and in vivo aimed to investigate the influence of DNA methylation of peroxisome proliferator activated receptor-α (PPAR-α) gene in non-alcoholic fatty liver disease (NAFLD) pathogenesis and to observe whether the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5-Aza-CdR) and the herbal medicine curcumin might reverse the effect both in vivo and in vitro. METHODS Steatotic hepatocyte model of cell lines and NAFLD rat models were established following protocols documented in previous studies. Subsequently, the models received 5-Aza-CdR and curcumin treatment. Morphological, histological and laboratory variables in each group were determined by routine methods, including PPAR-α mRNA expression by polymerase chain reaction (PCR), PPAR-α protein expression by Western blot and DNA methylation by pyrosequencing. RESULTS The steatotic hepatocyte model and NAFLD rat model were completely established. The expressions of PPAR-α mRNA and protein were significantly lower in the steatotic hepatocyte and NAFLD rat model groups than in the controls (P |
Databáze: | OpenAIRE |
Externí odkaz: | |
Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |