Role of SCD1 in mediating the effects of palmitic acid on ER stress, inflammation and apoptosis in goose primary hepatocytes.

Objective Unlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid (PA) tolerance of goose primary hepatocytes. Methods MTT was examined to reflect the effect of PA on hepatocytes viability, and quantitative PCR was used to detect the mRNA levels of several genes related to endoplasmic reticulum (ER) stress, inflammation, and apoptosis, and the role of SCD1 in PA tolerance of goose hepatocytes was explored using RNA interfere. Results Our results indicated that goose hepatocytes exhibited a higher tolerant capacity to PA than a human hepatic cell line (LO2 cells). In goose primary hepatocytes, the mRNA levels of fatty acid desaturation-related genes (SCD1 and FADS2) and fatty acid elongate enzyme-related gene (ELOVL6) were significantly upregulated with 0.6 mM PA treatment. However, in LO2 cells, expression of ER stress-related genes (XBP, BIP and ATF6), inflammatory response-related genes (IL-6, IL-1β and IFN-γ) and apoptosis-related genes (Bax, Bcl-2, Caspase-3 and Caspase-9) was significantly enhanced with 0.6 mM PA treatment. Additionally, siRNA-mediated downregulation of SCD1 significantly reduced the PA tolerance of goose primary hepatocytes under the treatment of 0.6 mM PA; meanwhile, the mRNA levels of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the PI3K/AKT, FoxO1, mTOR and AMPK pathways (AKT1, AKT2, FOXO1 and SIRT1), as well as the protein expression of cytochrome C and the apoptosis rate were upregulated. Conclusion In conclusion, our data suggested that SCD1 was involved in enhancing the PA tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.