SREBP1c silencing reduces endoplasmic reticulum stress and related apoptosis in oleic acid induced lipid accumulation

Objective: Sterol regulatory element binding protein 1c (SREBP1c) is one of the major transcription factors that involved in nonalcoholicfatty liver disease (NAFLD) development by increasing hepatic fatty acid and triglyceride synthesis. Our study aimed toinvestigate interaction SREBP1c with endoplasmic reticulum (ER) stress oleic (OA) induced lipid accumulation.Material Methods: Optimum droplet (LD) formation SREBP-1c induction were determined alpha mouse liver12 (AML12) hepatocytes following incubation different OA concentrations. To determine effect SREBP-1c, cellswere transfected siRNA specific for SREBP-1c. LD via Oil Red O andimmunblotting, respectively. Phospho IRE1, GRP78, CHOP, ATF6 JNK levels immunofluorescencestaining.Results: achieved at 0.5 mM oleat concentration. While silencingdecreased non-OA treated cells, no significant silencing was administration. Onthe other hand, cells reduced phospho ATF6, CHOP expressions.Conclusion: results suggest novel function can regulate ER response accumulation.