2008Chinese journal of integrated traditional and Western medicineRequires access

Protective effects of emodin(大黄素) on intestinal ischemia/reperfusion injury in rats

Liu Mu-li

Open publisher page 0 citations

Abstract

ObjectiveTo investigate the protective mechanism of emodin(大黄素) on intestinal mucosal injury induced by intestinal ischemia/reperfusion(I/R) in rats.Methods Thirty male Wistar rats were randomly divided into three groups,namely sham operation group(Group A),group of ischemia 45 minutes followed by reperfusion 6 hours(Group B),emodinpretreated group(Group C).The superior mesenteric artery was occluded and then released to produce the intestinal I/R model in rats.Group C was administrated emodin intravenously(2.5 mg/kg) before 30 minutes of the operation.In the sham operation group and model group,similar volume of normal saline was administered respectively.After 45 minutes of ischemia and 6 hours of reperfusion, the blood was collected from the inferior vena cava respectively in each group.Afterwards,the rats were sacrificed,and the mesenteric lymph node(MLN) and small intestinal tissues were taken for pathological analysis by light microscopy.The serum levels of intestinal fatty acid binding protein(IFABP),nitrogen monoxidum(NO),tumor necrosis factor-α(TNF-α),and the activities of malondialdehyde(MDA),superoxide dismutase(SOD),myeloperoxidase(MPO)in the small intestinal tissues were measured,and the rates of bacterial translocation(BT) in blood and MLN were examined at 6 hours after reperfusion in each group. Results The contents of IFABP,NO,TNF-α,MDA and MPO were significantly lower(all P0.01),SOD activity was significantly higher(P0.01) in group C than in group B.There was significant difference in the rate of BT between the group C and B(blood: 2/10 vs.8/10 rats;MLN: 3/10 vs.8/10 rats,both P0.05).Histological examination displayed that the damage of intestinal mucosa was less in group C than in group B.Conclusion Intestinal I/R may result in intestinal mucosal injury,the release of abnormal TNF-α,NO,reactive oxygen and activated polymorphonuclear leucocyte(PMN) may be involved in the mechanism.Emodin may protect intestinal mucosa against intestinal I/R injury,which may be associated with inhibiting the release of NO and TNF-α,ameliorating reactive oxygen damage,and alleviating the aggregation and activation of PMN.

About this research paper

What this paper is about

ObjectiveTo investigate the protective mechanism of emodin(大黄素) on intestinal mucosal injury induced by intestinal ischemia/reperfusion(I/R) in rats.Methods Thirty male Wistar rats were randomly divided into three groups,namely sham operation group(Group A),group of ischemia 45 minutes followed by reperfusion 6 hours(Group B),emodinpretreated group(Group C).The superior mesenteric artery was occluded and then released to produce the intestinal I/R model in rats.Group C was administrated emodin intravenously(2.5 mg/kg) before 30 minutes of the operation.In the sham operation group and model group,similar volume of normal saline was administered respectively.After 45 minutes of ischemia and 6 hours of reperfusion, the blood was collected from the inferior vena cava respectively in each group.Afterwards,the rats were sacrificed,and the mesenteric lymph node(MLN) and small intestinal tissues were taken for pathological analysis by light microscopy.The serum levels of intestinal fatty acid binding protein(IFABP),nitrogen monoxidum(NO),tumor necrosis factor-α(TNF-α),and the activities of malondialdehyde(MDA),superoxide dismutase(SOD),myeloperoxidase(MPO)in the small intestinal tissues were measured,and the rates of bacterial translocation(BT) in blood and MLN were examined at 6 hours after reperfusion in each group. Results The contents of IFABP,NO,TNF-α,MDA and MPO were significantly lower(all P0.01),SOD activity was significantly higher(P0.01) in group C than in group B.There was significant difference in the rate of BT between the group C and B(blood: 2/10 vs.8/10 rats;MLN: 3/10 vs.8/10 rats,both P0.05).Histological examination displayed that the damage of intestinal mucosa was less in group C than in group B.Conclusion Intestinal I/R may result in intestinal mucosal injury,the release of abnormal TNF-α,NO,reactive oxygen and activated polymorphonuclear leucocyte(PMN) may be involved in the mechanism.Emodin may protect intestinal mucosa against intestinal I/R injury,which may be associated with inhibiting the release of NO and TNF-α,ameliorating reactive oxygen damage,and alleviating the aggregation and activation of PMN.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

ObjectiveTo investigate the protective mechanism of emodin(大黄素) on intestinal mucosal injury induced by intestinal ischemia/reperfusion(I/R) in rats.Methods Thirty male Wistar rats were randomly divided into three groups,namely sham operation group(Group A),group of ischemia 45 minutes followed by reperfusion 6 hours(Group B),emodinpretreated group(Group C).The superior mesenteric artery was occluded and then released to produce the intestinal I/R model in rats.Group C was administrated emodin intravenously(2.5 mg/kg) before 30 minutes of the operation.In the sham operation group and model group,similar volume of normal saline was administered respectively.After 45 minutes of ischemia and 6 hours of reperfusion, the blood was collected from the inferior vena cava respectively in each group.Afterwards,the rats were sacrificed,and the mesenteric lymph node(MLN) and small intestinal tissues were taken for pathological analysis by light microscopy.The serum levels of intestinal fatty acid binding protein(IFABP),nitrogen monoxidum(NO),tumor necrosis factor-α(TNF-α),and the activities of malondialdehyde(MDA),superoxide dismutase(SOD),myeloperoxidase(MPO)in the small intestinal tissues were measured,and the rates of bacterial translocation(BT) in blood and MLN were examined at 6 hours after reperfusion in each group. Results The contents of IFABP,NO,TNF-α,MDA and MPO were significantly lower(all P0.01),SOD activity was significantly higher(P0.01) in group C than in group B.There was significant difference in the rate of BT between the group C and B(blood: 2/10 vs.8/10 rats;MLN: 3/10 vs.8/10 rats,both P0.05).Histological examination displayed that the damage of intestinal mucosa was less in group C than in group B.Conclusion Intestinal I/R may result in intestinal mucosal injury,the release of abnormal TNF-α,NO,reactive oxygen and activated polymorphonuclear leucocyte(PMN) may be involved in the mechanism.Emodin may protect intestinal mucosa against intestinal I/R injury,which may be associated with inhibiting the release of NO and TNF-α,ameliorating reactive oxygen damage,and alleviating the aggregation and activation of PMN.

Key concepts: Malondialdehyde, Myeloperoxidase, Medicine, Superoxide dismutase, Reperfusion injury, Saline, Ischemia, Ulinastatin

Related papers

Back to paper searchBrowse research topicsOriginal source
Protective effects of emodin(大黄素) on intestinal ischemia/reperfusion injury in rats — Research Paper | ScholarLens