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Acylation of anthocyanin with fatty acid has been extensively applied for the improvement of their lipophilicity and stability. However, their functionalities are not fully investigated. This work prepared cyanidin-3-O-glucoside–lauric acid ester (C3G–LA) and investigated its protective effect against oxidative stress in H2O2-induced human normal liver (LO2) cells. The results indicated that C3G–LA possessed notable antioxidant activity and better protective effect than its anthocyanin precursor cyanidin-3-O-glucoside (C3G). It protected the cells from H2O2-induced cell death and apoptosis by suppressing the overproduction of reactive oxygen species and malondialdehyde, restoring superoxide dismutase activity and ameliorating mitochondrial dysfunction and membrane damage. The increase in the expression levels of phosphorylated Akt, Nrf2, HO-1 and NQO1 further indicated that the antioxidant protective effect of C3G–LA involved the PI3K/Akt-mediated activation of the Nrf2–HO-1/NQO1 pathway. The findings indicated that, in addition to improve lipophilicity and stability, acylation of anthocyanin can enhance their anti-oxidative stress activity.

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 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide was examined to reflect the effect of PA on hepatocytes viability, and quantitative polymerase chain reaction 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 human hepatic cell line (LO2 cells). In goose primary hepatocytes, the mRNA levels of fatty acid desaturation-related genes (SCD1 and fatty acid desaturase 2) and fatty acid elongate enzyme-related gene (elongase of very long chain fatty acids 6) were significantly upregulated with 0.6 mM PA treatment. However, in LO2 cells, expression of ER stress-related genes (x box-binding protein, binding immunoglobulin protein, and activating transcription factor 6), inflammatory response-related genes (interleukin-6 [IL-6], interleukin-1β [IL-1β], and interferon-γ) and apoptosis-related genes (bcl-2-associated X protein, b-cell lymphoma 2, Caspase-3, and Caspase-9) was significantly enhanced with 0.6 mM PA treatment. Additionally, small interfering RNA (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 phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), forkhead box O1 (FoxO1), mammalian target of rapamycin and AMPK pathways (AKT1, AKT2, FoxO1, and sirtuin 1), 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.