Mitochondrial energy metabolism disorder and apoptosis: a potential mechanism of postoperative ileus.

AIM:To explore whether mitochondrial energy metabolism disorder and apoptosis of smooth muscle cells in intestinal muscularis are participated in pathogenesis of postoperative ileus (POI). METHODS:Rats were randomized into three groups: naive controls (NC) group, sham controls (SC) group and intestinal manipulation (IM) group. Gastrointestinal transits were analyzed. Reactive oxygen species (ROS), malondialdehyde (MDA) and adenosine triphosphatases (ATPases) activity in intestinal muscularis were determined. The levels of aldehyde dehydrogenase 2 (ALDH2), Bcl-2 and Bax in intestinal muscularis were measured by real-time PCR assays and western blot analysis. The levels of ATP, ADP and AMP in intestinal muscularis were determined by high performance liquid chromatography. Transmission electron microscopic was used to observe ultrastructure of smooth muscle cells and mitochondria in intestinal muscularis. RESULTS:Delayed gastrointestinal transitoccurred only in IM groups. After IM, increased levels of ROS and MDA were observed in intestinal muscularis. In IM groups, we also observed decreased levels of ALDH2 and Bcl-2/Bax ratio. The levels of ATP and ADP were decreased and level of AMP was increased in IM groups. The activity of ATPases was decreased in IM groups. Abnormal morphological architecture of smooth muscle cells and mitochondria were found in intestinal muscularis of IM groups. CONCLUSION:Our results suggest that mitochondrial energy metabolism disorder and apoptosis of smooth muscle cells in intestinal muscularis may participate in the development of POI.