Regulatory mechanisms of energy metabolism and inflammation in oleic acid-treated HepG2 cells from Lactobacillus acidophilus NX2-6 extract.

In this study, the cell-free extracts (CFE) of Lactobacillus acidophilus NX2-6 were utilized to treat oleic acid (OA)-induced hepatic steatosis. It was found that CFE treatment improved lipid metabolism in OA-induced hepatic steatosis model by downregulating several lipogenic genes but increasing expression levels of lipolysis-related genes. In addition, gene expression analysis revealed that CFE treatment promoted mitochondrial biogenesis and fission by upregulating the mRNA levels of PGC-1α, PGC-1β, Sirt1, NRF1, and Fis1. CFE treatment also increased protein expression of p-AMPKα, PGC-1α, ACOX1, and Sirt1 in OA-treated cells, suggesting that CFE possessed ability to improve energy metabolism. Furthermore, CFE treatment also reversed OA-induced oxidative stress by increasing CAT activity and protein level of Nrf-2 as well as reducing protein expression of ATF6, XBP1, GRP78, p50, and p-ERK, indicating that CFE could inhibit endoplasmic reticulum stress and sterile inflammation. Thus, L. acidophilus NX2-6 had potential to fight against NAFLD. PRACTICAL APPLICATIONS: Diet-induced hepatic steatosis is one of major public health concerns all over the world. Hepatic steatosis is accompanied by disregulation of lipid metabolism and energy metabolism, endoplasmic reticulum stress, oxidative stress as well as chronic inflammation. It is reported that probiotics are considered as emerging therapeutic strategy to alleviate hepatic steatosis. This study indicated potential applications of dead probiotics in the prevention of hepatic steatosis and development of functional foods.