| The energy metabolic disorders and peroxide damages in different tissues and organs is heterogeneous during hemorrhagic shock (HS), and its mechanisms remain unclear. Uncoupling protein-2 (UCP2),a protein playing a role in transporting proton in the inner membrane of mitochondria, can induce proton leak and decrease mitochondrial membrane potential. Thus, it can control ATP synthesis and restrain the production of oxygen free radicals (OFR) in mitochondria. There are studies indicating that UCP2 have an important effection on energy metabolic disorder and anti-peroxide damage, but no study illustrate the biological effect of UCP2 during HS at present. We suppose UCP2 may play a role in energy metabolic disorder and anti-peroxide damage, and which may associate with the vulnerablility of tissue damage during HS and resuscitation (HS/R).Object: To study the expression and the biological effect of UCP2 in mitochondria of intestinal epithelial,myocardical,skeletal muscle tissues during HS/R and explore the relationship between UCP2 and the different vulnerability to hypoxia or ischemia among the tissues mentioned above.Methods: The model of HS/R of rats were utilized in this experiment and intestinal epithelium,heart and skeletal muscle were obtained pre-shock,90min after HS (40mmHg),2h after HS/R,6h after HS/R,12h after HS/R,24h after HS/R. In order to observe the change of UCP2 and its functions during HS/R, the expression of UCP2 in mitochondria were determined by western-blot; The changes of mitochondrial membrane potential (MP) and the production of OFR were monitered by fluorospectrophotometry when theactivity of UCP2 were inhibited by GDP; The activity of XO and the content of MDA and ATP in the three tissues mentioned above were measured by spectrophotography and high performance liquid chromatograpy (HPLC).Results: (1) The expression of UCP2 is different in mitochondria of intestinal epithelia,heart,skeletal muscle. It is the highest in mitochondria of heart, then in skeletal muscle, the lowest in intestinal epithelia. The expression of UCP2 in mitochondria of intestinal epithelia ,heart,skeletal muscle increase 115%,33%,39%,respectively, during HS/R. (2) The mitochondrial MP rise up after the activity of UCP2 is inhibited with GDP during nomal condition and HS/R (p<0.01 vs non-GDP group); so does the production of OFR in mitochondria (p<0.05 vs non-GDP group, but except of mitochondria from intestinal epithelia and skeletal muscle during HS). (3) The activity of XO in epithelia is higher than it in skeletal muscle (p<0.05) but equal to heart; The activity of XO in the tissues of intestinal epithelia,heart and skeletal muscle increase 130%,76%,75%, respectively, during HS/R (p<0.05 vs baseline). (4) The content of MDA is not markedly different among above three tissues in normal condition, but its content in intestinal epithelia is higher than in heart or in skeletal muscle during HS/R(p<0.05); The content of MDA in the three tissues increase 210%,70%,87%, respectively, during HS/R (p<0.05 vs baseline). (5) The content of ATP in intestinal epithelia is lower than in heart or skeletal muscle during normal condition and HS/R (p<0.05). It falls to 21%,48%,52% respectively in intestinal epithelia,heart,skeletal muscler during HS ( p<0.01 vs baseline), and it recoveries to 56% (p<0.05 vs baseline) ,86% (p>0.05 vs baseline),73% (p<0.05 vs baseline) respectively after resuscitation.Conclusion: 1) The expression of UCP2 is different in mitochondria of intestinal epithelia,heart,skeletal muscle. It is the highest in mitochondria of heart, the second in mitochondria of skeletal muscle, the lowest in mitochondria of intestinal epithelia. The expression of UCP2 increases 115%,33%,39% respectively in mitochondria of intestinal epithelia,heart,skeletalmuscle during HS/R. 2) UCP2 can decrease MP and restrain the production of OFR, thus it involves in metabolic disfunction and anti-peroxide damage. 3) Intestinal epithelial energy metabolic disorder and peroxi... |
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