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Midkine is overexpressed in acute pancreatitis and promotes the pancreatic recovery in L‐arginine‐induced acute pancreatitis in mice
Author(s) -
Cheng Li,
Qiao Zhenguo,
Xu Chunfang,
Shen Jiaqing
Publication year - 2017
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.13681
Subject(s) - midkine , acute pancreatitis , medicine , pancreatitis , acinar cell , arginine , pancreas , pancreatic disease , pathogenesis , endocrinology , pathology , biology , growth factor , receptor , biochemistry , amino acid
Background and Aim Midkine (MK) is involved in the pathogenesis of numerous malignancies, but the expression and effect of MK in acute pancreatitis (AP) have not been well studied and documented. Methods In this study, the expression of MK was assayed in mice with L‐arginine‐induced AP. A recombinant human MK (rhMK) was introduced in this study to test the effect of MK on the L‐arginine‐induced AP. Serum amylase and lipase were assayed. Pancreas tissue samples were also collected for the evaluation of histological injury. Western blot and immunochemical staining of α‐amylase and proliferating cell nuclear antigen were applied for the study of acinar regeneration in the pancreas. Results The elevation of MK expression was found in mice with AP induced by L‐arginine. After rhMK administration, rhMK did not affect the severity of acute pancreatic injury in acute phase in L‐arginine‐induced pancreatitis in mice, in accordance with changes of serum amylase and lipase and the histological evaluation. But during the recovery phase, the area of remaining acinar cells was increased and the fibrosis was reduced in rhMK‐treated mice. Furthermore, the expression of proliferating cell nuclear antigen and α‐amylase was also upregulated after rhMK treatment. Conclusion Midkine is over‐expressed during AP in the animal model. Recombinant MK could promote the recovery of L‐arginine‐induced pancreatitis in mice. Therefore, MK may be involved in the regeneration of acinar cells in AP, and rhMK may be a possible therapeutic intervention for the repairment of AP.