YIFAN WANG1, HUAYU DIAO2, LINLING JU1, LIN CHEN1, YANGWANG3, ZHAOLIAN BIAN1, JIANGUO SHAO1*
1Nantong Institute of Liver Diseases, Nantong Third People’s Hospital, Nantong, Jiangsu 226006, P. R. China -2Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210023, P. R. China - 3School of medical, Nantong University, Nantong, Jiangsu 226006, P. R. China
Introduction: Acute pancreatitis (AP) is an inflammatory response with trypsin abnormal over-activation in the pancreas. Thematricellular proteinCysteine-rich protein 61 (CCN1) plays important roles in several inflammation diseases. However, the role of CCN1 inacute pancreatitis remains unclear. This work was aimed atinvestigating the protective effect of CCN1 on acute pancreati- tis and the potentialmechanism.
Materials and methods: The AP mouse model was induced byintraperitoneal injection(i.p.) of caerulein. Over-expression of
CCN1 was achieved by orbital intravenous injection of CCN1adenovirus. CCN1 mRNA and proteinlevels in pancreas were detected
by qPCR and western blots. Pancreatic tissue damage was evaluated and confirmed by Hematoxylin and Eosin staining H.&E. and serum amylase activity analysis. Leukocyte infiltration was observed and immunohistochemically stained.
Results: Caerulein-induced AP resulted inelevated serum amylase activity (p < 0.05). Histopathologic damage of pancreatic tissue in AP mice was significantly higher than saline group (p <0.05). Both mRNA and protein levels of CCN1 were decreased in AP group (p <0.05). Over-expressionof CCN1recovered CCN1 mRNA and protein levels. Pathological damage of pancreatic tissue was reduced in CCN1 over-expression APgroup (p <0.05). Over-expression of CCN1 in pancreas significantly decreasesneutrophils effu- sion but not macrophages in CCN1 over-expression AP mice (p <0.05).
Conclusions:Reduction of CCN1 may be associated with caerulein-induced AP development in mice. Further studies are nee- ded to investigate the effect of CCN1 in AP patients and the biochemical explanations for this phenomenon.
SAcute pancreatitis, CCN1, Inflammatory infiltration, Neutrophils, Caerulein