Expression and role of MLCK in small intestine mucosa in rats with acute necrotizing pancreatitis

Abstract

Objective To explore the expression and function of myosin light streptokinase (MLCK) in small intestine mucosa of acute necrotizing pancreatitis (ANP) rats. Methods Fifty-six male SD rats were randomly assigned to control group and ANP group. A rat model of ANP was reproduced by retrograde injection of 4% sodium taurocholate into the biliopancreatic duct, while the control group underwent a sham operation. The rats were sacrificed at 6th, 12th, 24th, 48th hour after ANP induction. Serum amylase、TNF α, IL 1β, diamine oxidase (DAO) were measured. The pathological scores in the pancreas and small intestine were observed. The ultrastructure and tight junction (TJ) changes in the small intestine mucosa were observed with an electron microscope. The localization and expression of MLCK in small intestine mucosa was determined by immunohistochemistry method. Results Compared to the control group, the serum amylase, TNF-α, IL-1β, DAO level, in the ANP group were all significantly increased; [(4 978±1 574)U/L vs (1 176±124))U/L, (47.88±15.85)μg/L vs (17.24±1.99)μg/L, (132.48±68.54)μg/L vs (23.51±6.44)μg/L, (95.96±30.84)μg/L vs (38.06±17.73)U/L at 12 h], and the pathology scores of pancreas and small intestine were both significantly elevated [12 h: (12.2±1.80) vs (4.68±0.35), (2.58±0.52) vs (0.58±0.26)] (P<0.05); the MLCK protein expression in small intestine mucosa was significantly increased in ANP group (12 h: 0.1863±0.0230 vs0.1636±0.0049), and the difference was statistically significant (P<0.05). The small intestine ultrastructure was seriously damaged and TJ was widened significantly in ANP Group. Conclusions The increased serum TNF alpha and IL-1β concentration and DAO activity and up-regulated MLCK protein expression in small intestine mucosa may damage the integrity of tight junction of intestinal epithelial cell and cause intestine mucosa barrier dysfunction. Key words: Pancreatitis, acute necrotizing; Tight junctions; Myosin-light-chain kinase; Intestine barrier