Abstract

The cell-free extract (CFE) of Lactobacillus acidophilus NX2-6 was used to treat oleic acid (OA)-exposed HepG2 cells. Biochemical analysis showed that CFE could reduce high levels of triglyceride, LDL-c, LDH, and MDA caused by OA treatment. RT-PCR and western blot analysis revealed that CFE distinctly decreased levels of Srebp-1c and FAS but elevated expression of CPT1. Fluorimetric analysis showed that CFE augmented mitochondrial membrane potential and mitochondrial content, and reduced ROS production induced by OA. Meanwhile, RT-PCR analysis also exhibited that CFE contributed to mitochondrial respiration by increasing expressions of respiratory complex subunits MTND1 , MTCO1 , MTATP6 and MTCYB . CFE also downregulated GRP58 , ATF6 , IREα , XBP1 and CHOP to alleviate ERS. Results also showed that CFE inhibited inflammatory responses through decreasing the levels of IL-1β and IL-6 and downregulating expression of NF-κB . Therefore, L. acidophilus possessed potentials to improve lipid metabolism, oxidative stress, mitochondrial dysfunction, ERS and inflammation in hepatocytes.