| Background:Severe acute pancreatitis is a common cause for hospitalization that carries a substantial burden of disease in China and worldwide. New methods to assess disease severity, innovative techniques for management of local complications, the importance of early recognition of pancreatic or extrapancreatic infection, and prevention of disease recurrence are still hot topics and problems which have not been sloved yet. Objective:To further investigate the complex pathogenesis of severe acute pancreatitis and its effects on renal injury,To investigate the effect of rosiglitazone,the highly selective peroxisome proliferator-activated receptor-y agonist,on renal injury of rats with severe acute pancreatitis and to investigate the protective mechanism of rosiglitazone,the highly selective peroxisome proliferator-activated receptor-y agonist,on renal injury of rats with severe acute pancreatitis. Methods:Fifty-four male Wistar rats were randomly divided into three groups:sham operation group (SO group),severe acute pancreatitis group (SAP group) and rosiglitazone pretreatment group (ROSI group). Acute pancreatitis model was induced by retrograde infusion of5%sodium taurocholate into the biliopancreatic duct.Rosiglitazone (6mg/kg) dissolved in10%DMSO were injected through the femoral vein30minutes piror to the operation. The rats of SO group and SAP group were injected partes aequales10%DMSO. Rats were sacrificed at3,12and24h after operation. We used the severe acute pancreatitis rat model which were induced by retrograde infusion of5%sodium taurocholate into the biliopancreatic duct. The level of serum amylase, serum creatinine, urea nitrogen, urinary albumin, urinary IgG and al-microglobulin were measured and analyzed statistically between control group and severe acute pancreatitis group at3,12and24h after operation.Kidney tissue samples were also stained respectively with hematoxylin and eosin for histopathological evaluation.Then the contents of NO and iNOS,the levels of NF-κB/P65,TNF-a and ICAM-1mRNA/proteins of kidney tissue samples were measured and analyzed statistically. Results:The level of serum amylase (SAP group) was2900±510U/L 3200±550U/L、5200±730U/L; The level of serum serum creatinine (SAP group) was142±22umol/L、196±19umol/L、316±18umol/L; The level of urea nitrogen(SAP group) was6.9±2.1mmol/L、11.7±1.4mmol/L、20.9±1.5mmol/L; The level of urinary albumin(SAP group) was93.8±9.6mg/L、170.5±16mg/L、208±20mg/L; The level of urinary IgG(SAP group) was18±3.2mg/L、18.3±1.6mg/L、23.5±2.4mg/L; The level of urinary al-microglobulin(SAP group) was14.2±0.9mg/L、18.3±0.5mg/L、34.1±0.82mg/L; all were significantly increased (P<0.05) after modeling.The level of The contents of NO(SAP group) was2.34±0.31mg/g、7.73±0.48mg/g、17.33±0.89mg/g; The level of NF-κB/p65(SAP group) was30648.11±2655.13、53654.63±3065.94、70546.85±5046.55; The level of TNF-(SAP group) was4.18±0.61、5.69±0.82、11.86±2.49; The level of ICAM-1(SAP group) was3.68±0.58、6.48±0.76、8.62±1.09, all were significantly increased (P <0.05) after modeling. The contents of NO(ROSI group) at12h,24h was4.10±0.62mg/g、6.09±0.79mg/g; The level of NF-κB/p65(ROSI group) at24h was30468.48±2684.59; The level of TNF-α (ROSI group) at24h was6.60±1.34; The level of ICAM-1(ROSI group) at24h was2.92±0.88;while lesser rise were detected in ROSI group at12h and24h (P<0.05) compared with which in SAP group. Conclusion:These data strongly suggest that renal injury can be induced by severe acute pancreatitis, which might provide further experimental evidence for guiding clinical diagnosis and treatment of acute pancreatitis. Renal injury can be induced by severe acute pancreatitis,while Rosiglitazone protects rats with severe acute pancreatitis from renal injury.Rosiglitazone protects rats with severe acute pancreatitis from renal injury with the mechanisms involving inhibiting NF-κB and then inhibiting TNF-α and ICAM-1production, thereby repressing the development of inflammation. |
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