Acute pancreatitis (AP) refers to
inflammation in the pancreas, which may lead to death in severe cases.
Coenzyme Q10 (Q10), generally known to generate energy, plays an important role as an
anti-oxidant and anti-inflammatory effector. Here, we showed the effect of Q10 on inflammatory response in murine AP model. For this study, we induced AP by injection of
cerulein intraperitoneally or pancreatic duct
ligation (PDL) in mice. The level of
cytokines and digestive
enzymes were measured in pancreas, and blood. All pancreatic tissues were excised for investigation such as histological changes, infiltration of immune cells. Administration of Q10 attenuated the severity of AP and its associated pulmonary complication as shown by reduction of acinar cell death, parenchymal
edema, inflammatory cell infiltration and alveolar thickening in both
cerulein-induced AP and PDL-induced AP. Moreover, reduction of the
cytokines such as
interleukin (IL)-1β,
IL-6 and
tumor necrosis factor (TNF)-α were observed in pancreas and pancreatic acinar cells by Q10. Furthermore, Q10 reduced the infiltration of immune cells such as monocytes and neutrophils and augmentation of
chemokines such as CC chemokine-2 (CCL2) and C-X-C chemokine-2 (CXCL2) in pancreas of AP mice. In addition, Q10 deactivates the phosphorylation of
extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal
kinase (JNK) in pancreas. In conclusion, these observations suggest that Q10 could attenuate the pancreatic damage and its associated pulmonary complications via inhibition of inflammatory
cytokines and inflammatory cell infiltration and that the deactivation of ERK and JNK by Q10 might contribute to the attenuation of AP.