Curcumin has been demonstrated to reduce markers of
inflammation during
acute pancreatitis (AP). However, the underlying mechanisms of the protective effects of
curcumin are unknown. In the present study the effects of
curcumin in an AP animal model and cell models was examined and the underlying mechanisms were investigated. An AP animal model was established by injection of 5%
sodium taurocholate into the biliopancreatic duct of rats, and the cell model was established by treatment with 0.5 nM
cerulein with an optimal concentration of
lipopolysaccharide in AR42J rat
pancreatic cancer cells.
Amylase activity and arterial blood gas composition were assessed by automatic biochemical and blood gas analyzers. Pathological alteration of the pancreas was determined by
hematoxylin and
eosin staining.
Interleukin (IL‑6),
tumor necrosis factor (TNF)‑α and C‑reactive
protein (CRP) levels were measured by ELISA. Cell viability was determined by Cell Counting Kit‑8 and
protein expression levels were assessed by western blotting.
Curcumin reduced the
ascites volume after 12 and 24 h, the weight of pancreas after 12, 24 and 36 h of surgery, but also attenuated injury to the pancreas. Serum expression levels of TNF‑α and CRP were reduced by
curcumin. In addition,
curcumin decreased the cell viability,
amylase activity and the phosphorylation of p38 in AR42J cells, but did not affect the intracellular levels of IL‑6 and TNF‑α.
Curcumin may lower the severity and inflammatory response via the mitogen‑activated
protein kinase‑signaling pathway, to some extent. However, future studies are required to fully understand the protective effects of
curcumin on AP.