Mu-Lin Liu1, Jia Zhang, Wei Wu, Rui-Lin Liu. 1. Department of gastrintestinal Surgery, Affiliated Hospital of Bengbu Medical College, Anhui, 233004 China. liumulin66@yahoo.com.cn
Abstract
OBJECTIVE: To investigate the mechanism of the injury of intestinal mucosal induced by intestinal ischemia-reperfusion and the protect effects of Urinary Trypsin Inhibitor (UTI). METHODS: Thirty male Wistar rats were randomly divided into three groups, the sham operation group (SO), ischemia 45 minutes and reperfusion 6 hours group (I/R), UTI-treated group (UTI). Using clamping and then releasing the superior mesenteric artery the model of intestinal ischemia-reperfusion in rats was made. UTI group was given UTI 2 x 10(4) U/KG by administering intravenously before 30 minutes of operation, while the group SO and I/R were intravenously injected with saline. Blood, intestinal tissue and lymph node were obtained after 6 hours of reperfusion. The level of intestinal fatty acid binding protein (IFABP), Tumor Necrosis Factor-alpha (TNF-alpha), Nitric Oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) and the rate of bacterial translocation (BT) in each group were examined. Intestinal tissue samples were also taken for histological analysis by light microscopy and electron microscopy. RESULTS: The content of IFABP, TNF-alpha, NO, MDA and MPO were significantly lower in group UTI than in group I/R [IFABP (520.87 +/- 75.41) pg/ml vs (493.57 +/- 136.35) pg/ml, NO (58.97 +/- 7.06) micromol/L vs (95.15 +/- 9.13) micromol/L, TNF-alpha (15.38 +/- 1.70) pg/ml to (23.55 +/- 4.34) pg/ml, MDA (4.5 +/- 1.1) nmol/mg vs (9.2 +/- 2.6) nmol/mg, MPO (1.98 +/- 0.22) U/g vs (3.02 +/- 0.55) U/g, SOD (77.08 +/- 7.14) U/mg vs (60.61 +/- 6.83) U/mg, P < 0.01]. There was significant difference in the rate of lymph node BT between the group UTI and I/R (P < 0.05). Histological changes showed that milder damage of intestinal mucosal in group UTI as to group I/R. CONCLUSION: Intestinal ischemia-reperfusion may result in intestinal mucosal damage, the mechanism may be involved in the release of abnormal TNF-alpha, NO, reactive oxygen and activated PMN; UTI can protect intestinal mucosal against intestinal ischemia-reperfusion injury, which may be associated with inhibiting the release of NO and TNF-a, ameliorating reactive oxygen damage, decreasing the aggregation and activation of PMN.
OBJECTIVE: To investigate the mechanism of the injury of intestinal mucosal induced by intestinal ischemia-reperfusion and the protect effects of Urinary Trypsin Inhibitor (UTI). METHODS: Thirty male Wistar rats were randomly divided into three groups, the sham operation group (SO), ischemia 45 minutes and reperfusion 6 hours group (I/R), UTI-treated group (UTI). Using clamping and then releasing the superior mesenteric artery the model of intestinal ischemia-reperfusion in rats was made. UTI group was given UTI 2 x 10(4) U/KG by administering intravenously before 30 minutes of operation, while the group SO and I/R were intravenously injected with saline. Blood, intestinal tissue and lymph node were obtained after 6 hours of reperfusion. The level of intestinal fatty acid binding protein (IFABP), Tumor Necrosis Factor-alpha (TNF-alpha), Nitric Oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) and the rate of bacterial translocation (BT) in each group were examined. Intestinal tissue samples were also taken for histological analysis by light microscopy and electron microscopy. RESULTS: The content of IFABP, TNF-alpha, NO, MDA and MPO were significantly lower in group UTI than in group I/R [IFABP (520.87 +/- 75.41) pg/ml vs (493.57 +/- 136.35) pg/ml, NO (58.97 +/- 7.06) micromol/L vs (95.15 +/- 9.13) micromol/L, TNF-alpha (15.38 +/- 1.70) pg/ml to (23.55 +/- 4.34) pg/ml, MDA (4.5 +/- 1.1) nmol/mg vs (9.2 +/- 2.6) nmol/mg, MPO (1.98 +/- 0.22) U/g vs (3.02 +/- 0.55) U/g, SOD (77.08 +/- 7.14) U/mg vs (60.61 +/- 6.83) U/mg, P < 0.01]. There was significant difference in the rate of lymph node BT between the group UTI and I/R (P < 0.05). Histological changes showed that milder damage of intestinal mucosal in group UTI as to group I/R. CONCLUSION: Intestinal ischemia-reperfusion may result in intestinal mucosal damage, the mechanism may be involved in the release of abnormal TNF-alpha, NO, reactiveoxygen and activated PMN; UTI can protect intestinal mucosal against intestinal ischemia-reperfusion injury, which may be associated with inhibiting the release of NO and TNF-a, ameliorating reactiveoxygen damage, decreasing the aggregation and activation of PMN.