An Experimental Study of the Protective Effects of Rosiglitazone on Lung Injury in Severe Acute Pancreatitis

ObjectiveTo investigate the protective effects and mechanisms of rosiglitazone on lung injury in severe acute pancreatitis(SAP).MethodsSeventy-two SD rats were randomized into three groups: sham operation(SO) group,SAP group and rosiglitazone-pretreated group. The model of SAP was induced by retrograde injection of 5% sodium tauro cholate into the bili-pancreatic duct in SD rats. Rats of rosiglitazone-pretreated group were given 10 mg/kg rosiglitazone in traperitoneally 30 min before inducing SAP. The amylase plasma levels, levels of TNF-α and p(O2), the myeloperoxidase(MPO) and the wet/dry ratio of lung tissue were measured. The expression of NF-κB in pulmonary tissues was assayed by im munohistochemistry. The expressions of TNF-α mRNA and intercellular adhesion molecule 1(ICAM-1) mRNA in pulmo nary tissues were detected by reverse transcript PCR(RT-PCR). The histopathological changes of pulmonary tissues were evaluated.ResultsCompared with SO group, the plasma levels of amylase and TNF-α, the intrapulmonary MPO were sig nificantly increased in SAP group(P0.05). The expression levels of NF-κB, TNF-α mRNA and ICAM-1 mRNA in lung tissue were also significantly increased in SAP group(P0.01). There were significantly lower levels of the above indicator in rosiglitazone-pretreated group than those of SAP group(P0.05). Compared with SO group, the lung wet/dryratio was sig nificantly higher at 6 h and 12 h in SAP group(P0.05). The values of lung wet/dry ratio were significantly lower at 6 h and12 h in rosiglitazone-pretreated group than those of SAP group(P0.05). The lung tissue damage was significantly reduced.The level of p(O2)was significantly decreased in SAP group than that of SO group(P0.05). The level of p(O2)was signifi cantly increased at 6 h and 12 h in rosiglitazone pretreated group than that of SAP group(P0.05).ConclusionRosigli tazone might have protective effects on SAP-related lung injury by inhibiting NF-κB and decreasing the production of TNF-α and ICAM-1in the lung tissues.