2010•Chin J PancreatolRequires access

Effect on blockade of MCP 1 in early course of experimental acute necrotizing pancreatitis

Li Ting Cheng, Guoyong Hu

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Abstract

Objective To investigate the potential role of MCP-1/CCL2 in experimental acute necrotizing pancreatitis (ANP) and complications. Methods 60 SD male rats were randomly divided into 3 groups: sham operation group ( n = 20 ), ANP group ( n = 20 ) and MCP-1 group ( n = 20 ). ANP model was induced by retrograde infusion of 3.5% sodium taurocholate, MCP-1 group received subcutaneous injection of MCP-1 antibody 0 h and 6 h after ANP induction. The serum levels of amylase, MCP-1, D-lactic acid,histological changes and the expression of MCP-1 mRNA of lung, small intestine and pancreas, the expression of MCP-1 protein in pancreas, MPO levels of small intestine MPO were determined. Results The serum levels of amylase, MCP-1, D-lactic acid in MCP-1 group at 12 h were (4666 ±412)U/L, (39.53 ±8.25)pg/ml and (6.3 ±2.2)mg/L, which were significantly lower than those in ANP group [ (9611 ±363)U/L, (63.42 ±9.32) pg/ml, (9.3 ± 2. 1 ) mg/L, P< 0.05 ) ]; the expression of MCP-1 mRNA in pancreas, small intestine and lung were 0.431 ± 0.009, 0. 211 ± 0.018 and 0.442 ± 0.017, which were significantly lower than those in ANP group [ (0.624 ±0. 010, 0. 523 ±0. 019 and 0. 569 ±0. 024, P <0.05) ]; the expression of MCP-1 protein in pancreas was 2.0 ± 0. 1, which was significantly lower than that in ANP group (4. 0 ± 0. 2, P <0.05). Lung and small intestine MPO were (11.1 ±3.0)U/g and ( 19.2 ±2.0)U/g, which were significantly lower than those in ANP group[(39.2±3.1)U/g and(13.1±2.1)U/g, P<0.05]. Conclusions Early blockade of MCP-1 not only attenuates the severity of ANP, but also decreases the degree of acute lung injury and intestine barrier dysfunction. Key words: Pancreatitis,acute necrotizing; Chemotactic factors; Monocyte chemotacite protein-1; Lung injuries; Enteral barrier

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Objective To investigate the potential role of MCP-1/CCL2 in experimental acute necrotizing pancreatitis (ANP) and complications. Methods 60 SD male rats were randomly divided into 3 groups: sham operation group ( n = 20 ), ANP group ( n = 20 ) and MCP-1 group ( n = 20 ). ANP model was induced by retrograde infusion of 3.5% sodium taurocholate, MCP-1 group received subcutaneous injection of MCP-1 antibody 0 h and 6 h after ANP induction. The serum levels of amylase, MCP-1, D-lactic acid,histological changes and the expression of MCP-1 mRNA of lung, small intestine and pancreas, the expression of MCP-1 protein in pancreas, MPO levels of small intestine MPO were determined. Results The serum levels of amylase, MCP-1, D-lactic acid in MCP-1 group at 12 h were (4666 ±412)U/L, (39.53 ±8.25)pg/ml and (6.3 ±2.2)mg/L, which were significantly lower than those in ANP group [ (9611 ±363)U/L, (63.42 ±9.32) pg/ml, (9.3 ± 2. 1 ) mg/L, P< 0.05 ) ]; the expression of MCP-1 mRNA in pancreas, small intestine and lung were 0.431 ± 0.009, 0. 211 ± 0.018 and 0.442 ± 0.017, which were significantly lower than those in ANP group [ (0.624 ±0. 010, 0. 523 ±0. 019 and 0. 569 ±0. 024, P <0.05) ]; the expression of MCP-1 protein in pancreas was 2.0 ± 0. 1, which was significantly lower than that in ANP group (4. 0 ± 0. 2, P <0.05). Lung and small intestine MPO were (11.1 ±3.0)U/g and ( 19.2 ±2.0)U/g, which were significantly lower than those in ANP group[(39.2±3.1)U/g and(13.1±2.1)U/g, P<0.05]. Conclusions Early blockade of MCP-1 not only attenuates the severity of ANP, but also decreases the degree of acute lung injury and intestine barrier dysfunction. Key words: Pancreatitis,acute necrotizing; Chemotactic factors; Monocyte chemotacite protein-1; Lung injuries; Enteral barrier

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Available abstract

Objective To investigate the potential role of MCP-1/CCL2 in experimental acute necrotizing pancreatitis (ANP) and complications. Methods 60 SD male rats were randomly divided into 3 groups: sham operation group ( n = 20 ), ANP group ( n = 20 ) and MCP-1 group ( n = 20 ). ANP model was induced by retrograde infusion of 3.5% sodium taurocholate, MCP-1 group received subcutaneous injection of MCP-1 antibody 0 h and 6 h after ANP induction. The serum levels of amylase, MCP-1, D-lactic acid,histological changes and the expression of MCP-1 mRNA of lung, small intestine and pancreas, the expression of MCP-1 protein in pancreas, MPO levels of small intestine MPO were determined. Results The serum levels of amylase, MCP-1, D-lactic acid in MCP-1 group at 12 h were (4666 ±412)U/L, (39.53 ±8.25)pg/ml and (6.3 ±2.2)mg/L, which were significantly lower than those in ANP group [ (9611 ±363)U/L, (63.42 ±9.32) pg/ml, (9.3 ± 2. 1 ) mg/L, P< 0.05 ) ]; the expression of MCP-1 mRNA in pancreas, small intestine and lung were 0.431 ± 0.009, 0. 211 ± 0.018 and 0.442 ± 0.017, which were significantly lower than those in ANP group [ (0.624 ±0. 010, 0. 523 ±0. 019 and 0. 569 ±0. 024, P <0.05) ]; the expression of MCP-1 protein in pancreas was 2.0 ± 0. 1, which was significantly lower than that in ANP group (4. 0 ± 0. 2, P <0.05). Lung and small intestine MPO were (11.1 ±3.0)U/g and ( 19.2 ±2.0)U/g, which were significantly lower than those in ANP group[(39.2±3.1)U/g and(13.1±2.1)U/g, P<0.05]. Conclusions Early blockade of MCP-1 not only attenuates the severity of ANP, but also decreases the degree of acute lung injury and intestine barrier dysfunction. Key words: Pancreatitis,acute necrotizing; Chemotactic factors; Monocyte chemotacite protein-1; Lung injuries; Enteral barrier

Key concepts: Internal medicine, Pancreas, Endocrinology, Amylase, Pancreatitis, Medicine, Small intestine, Lung

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