01 January 2008
The protective effect of resveratrol on the intestinal mucosal barrier in rats with severe acute pancreatitisRajiv Kumar JhaBCDEF, Ma Qing YongACDEG, Sha Huan ChenABCDEFG
Med Sci Monit 2008; 14(1): BR14-19 :: ID: 636055
Severe acute pancreatitis (SAP) can result in intestinal mucosal barrier (IMB) dysfunction. The aim of this study is to demonstrate the protective effect of resveratrol (RES) on the IMB in rats with SAP.
Material and Method
Fifty-four male Sprague-Dawley (SD) rats were randomly divided into three equal groups: a sham-operated group (SO), a severe acute pancreatitis group (SAP), and a resveratrol-treated group (RES), each group containing 6 rats which were evaluated at 3, 6, and 12 h. Serum endotoxin levels were determined by turbidimetry. The apoptosis rate of intestinal mucosal cells was detected by using the TUNEL method and the expressions of the apoptosis-related proteins Bcl-2 and Bax were observed using an immunohistochemical technique.
The serum endotoxin levels were significantly higher in the SAP group than in the SO group (P<0.05). The endotoxin levels of the RES group were lower than those of the SAP group at all the time-points (P<0.05). In the SAP group, pancreatic and intestinal mucosal congestion, edema, and inflammatory cell infiltration were apparent. In the RES group, pancreatic and intestinal morphological changes were alleviated at all time-points. The apoptotic cell index of the mucosal cells in the RES group was lower than that of the SAP group (P<0.05). In comparison with the SAP group, the RES group's expression of Bcl-2 increased and that of Bax decreased significantly (P<0.05).
An increase in intestinal mucosal cell apoptosis is involved in the intestinal mucosal dysfunction of SAP rats. Resveratrol could decrease endotoxin translocation and protect IMB function.
Keywords: Stilbenes - pharmacology, Proto-Oncogene Proteins c-bcl-2 - metabolism, Pancreas - pathology, Pancreatitis - physiopathology, Intestinal Mucosa - physiopathology, bcl-2-Associated X Protein - metabolism, Endotoxins - blood
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