Emodin Attenuates Autophagy Response to Protect the Pancreas From Acute Pancreatitis Failure

Objectives The aim of this study was to investigate the effects of emodin on attenuating autophagy response in acute pancreatitis (AP) models. Methods Acute pancreatitis was induced in Wistar rats by injecting 3% sodium taurocholate into the biliopancreatic duct. Emodin (40 mg/kg per day) was then given intragastrically, administrated 2 hours after AP induction. Rats were killed 24 hours after AP induction. The pancreatic injury was assessed using biochemical and histological approaches. Autophagosomes in pancreatic acinar cells were observed by electron microscopy. The expression levels of microtubule-associated protein 1 light chain 3 (LC3) B/A, beclin-1, and p62/SQSTM1 (p62) were detected by Western blotting, quantitative real-time polymerase chain reaction, and immunohistochemistry in pancreatic tissues. Results Compared with non–emodin-treated rats, the pathological injuries of the pancreas of emodin-treated rats were significantly alleviated, and autophagy vacuole formation was reduced within pancreatic acinar cells. Administration of emodin led to a reduction in the autophagy-associated protein level of LC3 (B/A) and p62 but not beclin-1. The transcript levels of LC3B, beclin-1, and p62 were decreased in the emodin-treated rats compared with non–emodin-treated rats. Conclusions Our data demonstrate that emodin plays a critical role in ameliorating AP, possibly by down-regulating autophagic protein levels.