2014•Zhonghua jizhen yixue zazhiRequires access

The expression of macrophage phenotype in kidney injury caused by severe acute pancreatitis

Sheng-Chun Dang, Shu Feng, Pingjiang Wang, Yao Shen, Jianxin Zhang

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Abstract

Objective To investigate the macrophages (Mφ) phenotype mechanism in acute kidney injury caused by severe acute pancreatitis (SAP).Methods Sixty-four male Wistar rats were randomly divided into control group (SO) and SAP group (n =32 in each group).SAP rat model was made by retrograde cholangiopancreatic injection of 5% sodium taurocholate.At 2,6,12 and 24 h after modeling,the samples of blood and kidney tissue were collected.The levels of blood urea nitrogen (BUN) and creatinine (Cr) were detected by using automatic biochemical analyzer.The expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA of kidney tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR).The levels of CD68,iNOS and Arg-1 were measured by Western blot.Results In the SAP group at each interval,BUN and Cr concentrations were significantly higher than those of the control group (P < 0.01,P < 0.05) ; Compared with the control group,the expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA in renal tissue of SAP group were significantly higher (P < 0.01,P < 0.05).In the SAP group,the levels of CD68,iNOS and Arg-1 were higher than those in the control group.Conclusions Inflammation and inflammatory imbalances may be pathological factors of acute kidney injury following SAP. Key words: Severe acute pancreatitis ;  Kidney injury;  Macrophages ;  CD68

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Objective To investigate the macrophages (Mφ) phenotype mechanism in acute kidney injury caused by severe acute pancreatitis (SAP).Methods Sixty-four male Wistar rats were randomly divided into control group (SO) and SAP group (n =32 in each group).SAP rat model was made by retrograde cholangiopancreatic injection of 5% sodium taurocholate.At 2,6,12 and 24 h after modeling,the samples of blood and kidney tissue were collected.The levels of blood urea nitrogen (BUN) and creatinine (Cr) were detected by using automatic biochemical analyzer.The expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA of kidney tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR).The levels of CD68,iNOS and Arg-1 were measured by Western blot.Results In the SAP group at each interval,BUN and Cr concentrations were significantly higher than those of the control group (P < 0.01,P < 0.05) ; Compared with the control group,the expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA in renal tissue of SAP group were significantly higher (P < 0.01,P < 0.05).In the SAP group,the levels of CD68,iNOS and Arg-1 were higher than those in the control group.Conclusions Inflammation and inflammatory imbalances may be pathological factors of acute kidney injury following SAP. Key words: Severe acute pancreatitis ;  Kidney injury;  Macrophages ;  CD68

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Available abstract

Objective To investigate the macrophages (Mφ) phenotype mechanism in acute kidney injury caused by severe acute pancreatitis (SAP).Methods Sixty-four male Wistar rats were randomly divided into control group (SO) and SAP group (n =32 in each group).SAP rat model was made by retrograde cholangiopancreatic injection of 5% sodium taurocholate.At 2,6,12 and 24 h after modeling,the samples of blood and kidney tissue were collected.The levels of blood urea nitrogen (BUN) and creatinine (Cr) were detected by using automatic biochemical analyzer.The expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA of kidney tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR).The levels of CD68,iNOS and Arg-1 were measured by Western blot.Results In the SAP group at each interval,BUN and Cr concentrations were significantly higher than those of the control group (P < 0.01,P < 0.05) ; Compared with the control group,the expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA in renal tissue of SAP group were significantly higher (P < 0.01,P < 0.05).In the SAP group,the levels of CD68,iNOS and Arg-1 were higher than those in the control group.Conclusions Inflammation and inflammatory imbalances may be pathological factors of acute kidney injury following SAP. Key words: Severe acute pancreatitis ;  Kidney injury;  Macrophages ;  CD68

Key concepts: Acute pancreatitis, Medicine, CD68, Kidney, Creatinine, Acute kidney injury, Pancreatitis, Internal medicine

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