Emodin attenuates calcium overload and endoplasmic reticulum stress in AR42J rat pancreatic acinar cells

The aim of the present study was to investigate the protective effects of emodin against calcium overload and endoplasmic reticulum (ER) stress in an acute pancreatitis model in vitro. AR42J rat pancreatic acinar cells treated with cerulein (10(-7) M) and lipoplysaccharide (LPS; 10 mg/l) were used to mimic acute pancreatitis in vitro. The amylase activity in cellular lysates and culture media was detected by spectrophotometry. The level of cytosolic calcium was measured by laser confocal microscopy. Cell apoptosis and necrosis were examined by flow cytometry. Reverse transcription-polymerase chain reaction was used to determine the mRNA expression of ER chaperone immunoglobulin-binding protein (Bip) and downstream molecules, including protein kinase-like ER kinase (PERK), activation transcription factor 6 (ATF6) and inositol-requiring protein 1 (IRE1). The results showed that emodin significantly reduced the expression and release of amylase, attenuated calcium overload and decreased the mRNA expression of Bip, PERK, ATF6 and IRE1 which was significantly elevated in AR42J cells treated with cerulein and LPS. Emodin also reduced cell apoptosis and necrosis. Therefore, the results of the present study indicate that emodin protects against AR42J cell injury caused by cerulein and LPS. These effects may be associated with reduced calcium overload and inhibited ER stress responses.