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Endoplasmic reticulum (ER) stress plays a pivotal role in the progression of steatohepatitis. 5-aminolevulinic acid (5-ALA), a precursor in the heme biosynthetic pathway, has recently been reported to induce heme oxygenase (HO)-1. HO-1 exerts important cytoprotective actions. In this study, we aimed to explore the therapeutic potential of 5-ALA on palmitate-induced ER stress and lipoapoptosis. Huh-7 cells were treated with palmitic acid (PA) (800 μM) to induce steatosis for eight hours. Steatosis was evaluated by Lipi-green staining. 5-ALA (200 μM) was added with PA. The gene expression levels of the nuclear factor erythroid 2–related factor 2 ( NRF2 ),  HO-1 , Glucose-regulated protein 78 ( GRP78 ), activating transcription factor 6 ( ATF6 ), PKR-like endoplasmic reticulum kinase ( PERK ), inositol-requiring enzyme 1 ( IRE1 ), C/EBP homologous protein ( CHOP ), and B-cell lymphoma 2 ( BCL-2 ) were evaluated by RT-PCR. Caspase-3/7 activity was evaluated by fluorescein active Caspase-3/7 staining. Cell death was evaluated by Annexin V/SYTOX green staining. PA significantly induced steatosis and increased  GRP78  expression in Huh-7 cells. 5-ALA significantly induced  HO-1  and decreased  GRP78  expression.  ATF6  was subsequently decreased. However,  NRF2  and  CHOP  expression were not altered. Anti-apoptotic  BCL-2  expression significantly increased, and Caspase 3/7 activity and cell death also decreased. 5-ALA has a therapeutic potential on hepatic steatosis by suppressing ER stress and lipoapoptosis by attenuating  GRP78  via  HO-1  induction.

5-Aminolevulinic Acid Attenuates Glucose-Regulated Protein 78 Expression and Hepatocyte Lipoapoptosis via Heme Oxygenase-1 Induction