Protective effects of Lactobacillus acidophilus NX2-6 against oleic acid-induced steatosis, mitochondrial dysfunction, endoplasmic reticulum stress and inflammatory responses

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.

Keywords

• Lactobacillus acidophilus
• Cell-free extract
• Mitochondrial dysfunction
• Endoplasmic reticulum stress
• Inflammation