Hong-Shan L.,Henan Provincal Hospital |
Chen'En P.,Xi'an Jiaotong University |
Huanzhou X.,Henan Provincal Hospital |
Deyu L.,Henan Provincal Hospital |
And 3 more authors.
Journal of Animal and Veterinary Advances | Year: 2011
To investigate effect of p38 mAPK inhibitor on adhesion molecule expression and microvascular permeability of renal injury in a rat model of acute necrotizing pancreatitis. Sixty pathogen free male Sprague-Dawley rats were randomly divided into the sham group, acute necrotizing pancreatitis group (ANP group) and ANP group of rats with treatment of SB203580 (SB203580, 0.5 mg kg-1, iv). The rats were sacrificed at 1, 3, 6 and 12 h after operation. The serum of BUN, Cr, β32-MG, serum and renal tissue of TNF-a were determined. The expressions of pho-p38 MAPK in the pancreas and renal tissue of SAP rat were determined by immunohistochemical technique and the expression of ICAM-1 mRNA was detected through RT-PCR. The pancreas and renal tissue samples were stained with HE for histopathological evalution. The Serum of BUN, Cr and β32-MG, serum and renal tissue of TNF-a, the expression and pho-p38 MAPK and ICAM-1 mRNA of pancreas and renal tissure in ANP group and SB group were more significantly increased than those of the sham group (p<0.05). Moreover, those of SB group were more significantly reduced than those of SAP group (p<0.05). The renal sections from SB203580-treated groups displayed significantly less proximal tubule cell necrosis than those of ANP group. The activation and over expression of pho-p38 MAPK and ICAM-1 mRNA of renal tissue may be one of the reasons for renal injury in ANP and SB203580 can be used to treat the ANP associated renal injury through down regulating the expression of pho-p38 MAPK and ICAM-1 mRNA in renal tissue. © Medwell Journals, 2011.