Effect of mesenchymal stem cells on small intestinal injury in a rat model of acute necrotizing pancreatitis

Fengchun Lu,Feng Wang,Zhiyao Chen,Heguang Huang

doi:10.1186/s13287-017-0471-z

Fengchun Lu, Feng Wang + Show 2 more

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https://doi.org/10.1186/s13287-017-0471-z

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Abstract

BackgroundAcute necrotizing pancreatitis (ANP) is often complicated by multiple organ failure. The small intestine is frequently damaged during ANP. Capillary leakage in multiple organs during ANP is one of the most important causes of multiple organ dysfunction. Damage to the capillary endothelial barrier and impaired water transportation could lead to capillary leakage in ANP.MethodsSprague–Dawley (SD) rats were randomized into a control group, the ANP group, the culture media-treated group, or the bone marrow-derived mesenchymal stem cell (BMSC)-treated group (30 rats in each group). Ten rats in each group were sacrificed at 6, 12, and 24 h after induction of experimental models. Serum, ascites, pancreatic, and small intestinal samples were collected. The levels of serum and ascites albumin and amylases were measured, pancreatic histology was assessed, and the connection changes between vessel endothelial cells were evaluated using scanning electron microscopy (SEM). Capillary leakage in small intestinal tissue was observed visually by tracking fluorescein isothiocyanate (FITC)-albumin, and was measured by the Evans blue extravasation method. The location and expression of aquaporin 1 (AQP1) in the small intestine was analyzed using immunohistochemistry, real-time polymerase chain reaction (PCR), and Western blot.ResultsThe outcomes showed that the level of serum and ascites amylase is elevated. Conversely, the level of serum albumin is decreased while ascites albumin is elevated. There is damage to pancreatic tissue, and the small intestinal capillary endothelial barrier was aggravated. Furthermore, the expression of AQP1 was reduced significantly after induced ANP. Following treatment with MSCs, the elevation of amylase and the decrease of serum albumin were inhibited, the damage to pancreatic tissue and the level of small intestinal capillary leakage was alleviated, and the downregulation of AQP1 was reversed.ConclusionsIn conclusion, MSC therapy could alleviate small intestinal injury in rats with ANP, the mechanism of which might be related to reduction of damage to the small intestinal capillary endothelial barrier, and increased expression of AQP1 in the small intestine.

Highlights

Acute necrotizing pancreatitis (ANP) is often complicated by multiple organ failure
We examined the changes of the small intestinal capillary endothelial barrier and aquaporin 1 (AQP1) expression in the rat model of ANP, and explored whether Mesenchymal stem cell (MSC) have a protective effect on small intestinal injury induced by ANP through their impact on the capillary endothelial barrier and expression of AQP1 in the small intestine
High expression of CD 29/90 and low expression of CD 34/45 confirmed that these cells were MSCs (Fig. 1c–f )

Summary

Introduction

Acute necrotizing pancreatitis (ANP) is often complicated by multiple organ failure. Damage to the capillary endothelial barrier and impaired water transportation could lead to capillary leakage in ANP. Acute necrotizing pancreatitis (ANP) is a challenging disease with high morbidity and mortality, often complicated by multiple organ failure. Capillary leakage occurs in the early phase of ANP. Capillary leakage in multiple organs during ANP is one of the most important causes of multiple organ dysfunction. The small intestine is frequently damaged during ANP. Intestinal edema, abundant amylase and bloody ascites, and intestinal barrier functional disturbances can be found in ANP.

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