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Objective This study investigated the effect of percutaneous catheter drainage (PCD) on pancreatic injury in severe acute pancreatitis (SAP) rats. Methods Sixty Wistar rats were equally randomized into three groups: a sham operated control group, an SAP control group, and a PCD group. The levels of inflammatory cytokines, the activity of group II phospholipase A2 (PLA2) in blood and ascitic fluid, and the pancreas level of group II PLA2 and trypsin activity were measured 24 h after the operation. The apoptosis of the pancreatic cells, the expression of cycloxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), active caspase-3, Bcl-2 and Bax in the pancreas was detected. Pancreatic pathological changes were observed. Results The levels of proinflammatory cytokines, the activity of group II PLA2 and trypsin activity in pancreas in the SAP group were higher than those in the PCD group. The histopathological results revealed that the pancreatic injury was alleviated in the PCD group. The expression of COX-2 and iNOS in the pancreatic tissue in the SAP control rats was higher than that in the PCD rats. The expression of Bcl-2 was decreased and the expression of active caspase-3 and Bax was increased in the pancreas of PCD rats. The apoptosis index of the pancreatic cells in the PCD rats was higher than that in the SAP control rats. Conclusion PCD can relieve SAP-induced pancreatic injury by inhibiting inflammatory reactions, and promoting apoptosis of pancreatic cells. [ABSTRACT FROM AUTHOR]

Background and Aim Oxidative stress and inflammation play important roles in the progression from simple fatty liver to non-alcoholic steatohepatitis ( NASH). The aim of this work was to investigate whether treatment with hydrogen sulfide ( H2S) prevented NASH in rats through abating oxidative stress and suppressing inflammation. Methods A methionine-choline-deficient ( MCD) diet rat model was prepared. Rats were divided into three experimental groups and fed for 8 weeks as follows: (i) control rats; (ii) MCD-diet-fed rats; (iii) MCD-diet-fed rats treated with NaHS (intraperitoneal injection of 0.1 mL/kg/day of 0.28 mol/L NaHS, a donor of H2S). Results MCD diet impaired hepatic H2S biosynthesis in rats. Treatment with H2S prevented MCD-diet-induced NASH, as evidenced by hematoxylin and eosin staining, reduced apoptosis and activities of alanine aminotransferase and aspartate aminotransferase, and attenuated hepatic fat accumulation in rats. Treatment with H2S abated MCD-diet-induced oxidative stress through reducing cytochrome p4502 E1 expression, enhancing heme oxygenase-1 expression, and suppressing mitochondrial reactive oxygen species formation, and suppressed MCD-diet-induced inflammation through suppressing activated nuclear factor κB signaling and reducing interleukin-6 and tumor necrosis factor α expressions. In addition, treatment of MCD-diet fed rats with H2S had a beneficial modulation on expression profiles of fatty acid metabolism genes in livers. Conclusions Treatment with H2S prevented NASH induced by MCD diet in rats possibly through abating oxidative stress and suppressing inflammation. [ABSTRACT FROM AUTHOR]