Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2007
[Role of cyclooxygenase-2 in pulmonary microcirculation disorder in rats with acute pancreatitis].
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Zhou Ye-Jiang, Xiong Yu-Xia, Zhou Tong, Fan Wei, Wu Xiao-Ting
Аннотация
OBJECTIVE: To identify the expression of Cyclooxygenase-2 (Cox-2) in lung tissues and its potential role in pulmonary microcirculation disorder in rats with acute pancreatitis.
METHODS: The acute hemorrhagic and necrotic pancreatitis (AHNP) model was induced by the standard retrograde infusion of bilio-pancreatic duct with 4% sterile sodium taurocholate solution in Sprague-Dawley rats. The rats were randomly allocated into sham surgery group, AHNP group, and prophylactic celecoxib treated AHNP (C+ AHNP) group. The HE, phosphotungstic acid hematain (PTAH) and immunohistochemistrical (IHC) staining were employed to assess the dynamical alterations and interrelations of the histopathology, density of micro-thrombus and Cox-2 expression of lung tissue respectively over a time course of 3, 6, 12 and 24 hours.
RESULTS: A significant and progressing increase in histopathologic scoring and Cox-2 expression in the lung tissues were found. There was a positive correlation between the Cox-2 expression and the histopathological scoring. A significant increase of pulmonary micro-thrombosis was detected at the early stage of the rat AHNP induced by sodium taurocholate, and the density of micro-thrombus was positively associated with the histopathological scoring. The prophylactic treatment with celecoxib, a highly selective inhibitor of Cox-2, attenuated the changes in histopathology, pulmonary micro-thrombosis and Cox-2 expression (P < 0.05). The down-regulated intensity of the Cox-2 expression by celecoxib was positively correlated with the improvement of the histopathology injury, but not with the change of the pulmonary micro-thrombosis.
CONCLUSION: The pulmonary microcirculation dysfunction caused by micro-thrombosis is an early event or even an enabler of the development of APALI. The over-expression of Cox-2 may have promoted the procoagulant activity which plays a key role in the development of pulmonary thrombus.
METHODS: The acute hemorrhagic and necrotic pancreatitis (AHNP) model was induced by the standard retrograde infusion of bilio-pancreatic duct with 4% sterile sodium taurocholate solution in Sprague-Dawley rats. The rats were randomly allocated into sham surgery group, AHNP group, and prophylactic celecoxib treated AHNP (C+ AHNP) group. The HE, phosphotungstic acid hematain (PTAH) and immunohistochemistrical (IHC) staining were employed to assess the dynamical alterations and interrelations of the histopathology, density of micro-thrombus and Cox-2 expression of lung tissue respectively over a time course of 3, 6, 12 and 24 hours.
RESULTS: A significant and progressing increase in histopathologic scoring and Cox-2 expression in the lung tissues were found. There was a positive correlation between the Cox-2 expression and the histopathological scoring. A significant increase of pulmonary micro-thrombosis was detected at the early stage of the rat AHNP induced by sodium taurocholate, and the density of micro-thrombus was positively associated with the histopathological scoring. The prophylactic treatment with celecoxib, a highly selective inhibitor of Cox-2, attenuated the changes in histopathology, pulmonary micro-thrombosis and Cox-2 expression (P < 0.05). The down-regulated intensity of the Cox-2 expression by celecoxib was positively correlated with the improvement of the histopathology injury, but not with the change of the pulmonary micro-thrombosis.
CONCLUSION: The pulmonary microcirculation dysfunction caused by micro-thrombosis is an early event or even an enabler of the development of APALI. The over-expression of Cox-2 may have promoted the procoagulant activity which plays a key role in the development of pulmonary thrombus.