Akademik Veri Yönetim Sistemi
Turkish Journal of Biochemistry, 2025 (SCI-Expanded, Scopus, TRDizin)
Objectives: We aimed to evaluate the effects of L-carnitine, taurine, and vitamin E in steatosis, protein oxidation, endoplasmic reticulum (ER) stress, and paraoxonase enzymes in fatty acid-induced NAFLD models. We also investigated the role of AMP-activated protein kinase (AMPK) in these effects. Methods: HepG2 cells were incubated for 24 h with 1 mM palmitic acid (PA) or a 1 mM oleic acid (OA) and PA mixture to generate NAFLD models, representing acute lipotoxicity and benign chronic steatosis, respectively. L-carnitine, taurine, or vitamin E was applied together with fatty acids. Also, tunicamycin (ER stress inducer), 4-phenylbutyrate (ER stress inhibitor), or compound C (AMPK inhibitor) treatments were used. MTT test was used to evaluate cell viability. Measurement of triglyceride levels and oil red O staining of cells were used to determine steatosis. Protein carbonyl (PC), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), PON1-3, phosphorylated/total AMPK were evaluated by Western blotting. Results: L-carnitine, taurine, and vitamin E reduced triglyceride levels in both models. Taurine and vitamin E also decreased PC levels in both models. Additionally, vitamin E lowered 1 mM PA-induced ATF4 and CHOP levels. Neither the models nor the treatments with L-carnitine, taurine, and vitamin E caused significant changes in PON1-3 or phosphorylated/total AMPK levels. Conclusions: L-carnitine, taurine, and vitamin E attenuated lipid accumulation, with vitamin E demonstrating superior efficacy by significantly reducing both protein oxidation and ER stress. No changes in PON1-3 levels or AMPK phosphorylation were observed in the models or treatments under the conditions of this study.