This study aimed to investigate the protective effect of
emodin on endoplasmic reticulum (ER) stress in rats with severe
acute pancreatitis (SAP) and the underlying molecular mechanism. Sprague-Dawley male rats were randomly divided into
sham operation group, SAP model group, and
emodin treatment group. SAP was constructed through injecting
sodium taurocholate into pancreatic and biliary duct in rats. Half an hour before establishing the animal model,
emodin or
sodium carboxymethylcellulose was intragastrically administrated to the rats in respective group. Rats were killed at 3, 6, and 12 h postdisease induction. The
amylase,
tumor necrosis factor-alpha (TNF-α) and
interleukin-6 (IL-6) levels in serum, pancreatic histopathology, acinar ER ultrastructure,
protein expression of Bip, IRE1α,
TRAF2, ASK1, p-JNK, and p-p38 MAPK in pancreas were examined.
Sodium taurocholate induced pancreatic injury and ER lumen dilated in exocrine pancreas in rats at 3-, 6-, and 12-h time points. ER stress transducers Bip, IRE1α, and their downstream molecules
TRAF2, ASK1 in
pancreatitis were upregulated. Furthermore, phosphorylation of JNK and p38MAPK in pancreas was increased, which induced high expression level of inflammatory
cytokines such as TNF-α and
IL-6. Treatment with
emodin obviously ameliorated pancreatic injury and decreased the release of
amylase and inflammatory
cytokines. Further studies showed that
emodin significantly decreased the expression of Bip, IRE1α,
TRAF2, and ASK1, inhibited phosphorylation of JNK and
p38 MAPK in pancreas in rats at all time points.
Emodin could reduce pancreatic injury and restrain inflammatory reaction in SAP rats partly via inhibiting ER stress transducers IRE1α and its downstream molecules.