The role of nuclear factor kappaB in intestine injury induced by hepatic ischemia reperfusion was investigated. Eighteen male Wistar rats were divided into 3 groups randomly: sham operation group (group A), hepatic ischemia reperfusion group (group B) and hepatic ischemia reperfusion plus pyrrolidine dithiocarbamate (PDTC) group (group C). The rats in group A were only subjected to laparotomy, those in group B underwent partial hepatic ischemia reperfusion (ischemia for 1 h and reperfusion for 2 h) and those in group C underwent the same procedure as that of group B but received PDTC 200 mg/kg i.v. before and after ischemia. After reperfusion, tissues of jejunum and venous blood were obtained for measurement of TNF-alpha, MDA and MPO. The levels of TNF-alpha in jejunum and venous blood, the levels of MPO in jejunum in group B were significantly higher than those in group A and group C (P<0.05). There was no significant different in the levels of MDA between group B and group C. The severity of histological intestinal injury in group B and group C was similar. Hepatic ischemia reperfusion caused intestine injury, NF-kappaB may play an important role in this course and the targeting of upstream components of the inflammatory response, such as NF-kappaB, may have important therapeutic applications.
Animals ; Intestines ; pathology ; Liver ; blood supply ; metabolism ; Male ; NF-kappa B ; biosynthesis ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

The role of nuclear factor kappaB in intestine injury induced by hepatic ischemia reperfusion was investigated. Eighteen male Wistar rats were divided into 3 groups randomly: sham operation group (group A), hepatic ischemia reperfusion group (group B) and hepatic ischemia reperfusion plus pyrrolidine dithiocarbamate (PDTC) group (group C). The rats in group A were only subjected to laparotomy, those in group B underwent partial hepatic ischemia reperfusion (ischemia for 1 h and reperfusion for 2 h) and those in group C underwent the same procedure as that of group B but received PDTC 200 mg/kg i.v. before and after ischemia. After reperfusion, tissues of jejunum and venous blood were obtained for measurement of TNF-alpha, MDA and MPO. The levels of TNF-alpha in jejunum and venous blood, the levels of MPO in jejunum in group B were significantly higher than those in group A and group C (P<0.05). There was no significant different in the levels of MDA between group B and group C. The severity of histological intestinal injury in group B and group C was similar. Hepatic ischemia reperfusion caused intestine injury, NF-kappaB may play an important role in this course and the targeting of upstream components of the inflammatory response, such as NF-kappaB, may have important therapeutic applications.
Intestines/*pathology ; Liver/*blood supply ; Liver/metabolism ; NF-kappa B/*biosynthesis ; Random Allocation ; Rats, Wistar ; Reperfusion Injury/*metabolism

OBJECTIVETo observe the protective effect of electroacupuncture (EA) at "Zusanli" (ST 36) on inflammatory injury induced by intestinal ischemia/reperfusion (I/R) in rats.

METHODSForty-eight Wistar rats were randomly divided into a sham injury group, a model group, an EA group and a sham EA group, 12 rats in each group. Intestinal I/R rat models were established by method of clamping with occlusion of superior mesenteric artery (SMA) for 45 min followed by reperfusion. The EA group was treated with EA (2.5 mA, 2 Hz/100 Hz, 0.5 h) at "Zusanli" (ST 36) 30 min before reperfusion, and at the same time, the sham EA group was treated with fast insertion at two non-meridian acupoints on skin surface (2 cm horizontally away from linea alba abdominis and about 5 cm paralleled to cartilago ensiformis downward). No interventions were added on the sham injury group and the model group. The degree of pathological injury in intestines, water rate of intestines, diamine oxidase (DAO) activity and intestinal mucosal blood flow (IMBF) were examined at 1 h and 3 h after reperfusion.

RESULTSAt 1 h and 3 h after reperfusion, the intestinal pathological injury in EA group was significantly attenuated compared with that in model group, and the intestinal water rate of (74.00 +/- 2.11)% and (78.78 +/- 0.80)% in EA group were significantly lower than (80.69 +/- 1.66)% and (83.17 +/- 2.08)% in model group (both P < 0.01), but DAO of (68.83 +/- 4.31) U/L and (47.84 +/- 5.57) U/L as well as IMBF of (152 +/- 5.8) PU and (139.8 +/- 6.1) PU in EA group were significantly higher than DAO of (32.86 +/- 4.72) U/L, (17.01 +/- 2.96) U/L as well as IMBF of (124.7 +/- 8.3) PU and (89.4 +/- 13.2) PU in model group (all P < 0.01). Meanwhile, the above mentioned changes in sham EA group showed no significant differences compared with those in model group (all P > 0.05).

CONCLUSIONElectroacupuncture can not only reduce the inflammatory injury induced by intestinal IR but also increase intestinal blood supply so as to protect the intestine function.

Acupuncture Points ; Amine Oxidase (Copper-Containing) ; metabolism ; Animals ; Electroacupuncture ; Inflammation ; therapy ; Intestines ; blood supply ; metabolism ; pathology ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury ; therapy

OBJECTIVETo investigate the sheltering effects of ω-3 polyunsaturated fatty acid (ω-3PUFA) and lymphatic drainage on distant organs in intestinal ischemia-reperfusion injury in rats.

METHODSForty-eight healthy Sprague-Dawley (SD) male rats (SPF grade) were randomly divided into 3 groups (16 rats in each group): normal diet group (N), enteral nutrition group (EN), enteral nutrition and ω-3PUFA group(PUFA group). Each group was divided into lymphatic drainage (I/R + D) group and no-drainage (I/R) group (n = 8). Each rats received gastrostomy. After given different nutrition for five days, the rats subjected to 60 min ischemia and 120 min reperfusion injury of the superior mesenteric artery. When the rats subjected to ischemia-reperfusion injury, drained intestinal lymph for 180 min in the I/R + D group. The serum level of alanine aminotransferase (ALT) and level of myeloperoxidase (MPO), nitric oxide (NO), total of nitric oxide synthase (tNOS), inducible nitric oxide synthase (iNOS) of lung were detected. The organ injury of lung and liver and the expression of high mobility group box 1(HMGB1, the endogenous ligand of TLR4) in these organs were investigated too.

RESULTSThe serum level of ALT in PUFA I/R + D and I/R group and EN I/R + D group were significantly lower than that in normal diet I/R group: (46 ± 20), (53 ± 15), (46 ± 21) and (100 ± 60) U/L (P < 0.05), respectively. The level of MPO, NO, tNOS, iNOS in lung in the I/R + D group were significantly lower than those in I/R group (P < 0.05): MPO (0.73 ± 0.15):(0.85 ± 0.10) unit/grams wet slice; NO (0.72 ± 0.51):(1.79 ± 1.32) µmol/gprot; tNOS (0.46 ± 0.15):(0.78 ± 0.27) U/mgprot; iNOS (0.06 ± 0.04):(0.11 ± 0.07) U/mgprot, respectively. The level of tNOS in PUFA I/R group was significantly lower than that in normal diet I/R group: (0.56 ± 0.13):(0.78 ± 0.27) U/mgprot (P < 0.05). MPO, NO, INOS levels in PUFA group were reduced compared with those in EN and normal diet group. HE stained sections and HMGB1 immunohistochemistry results showed that the organ injury in I/R group was severer than that in I/R + D group. The expression of HMGB1 increased in I/R group. The organ injury and the expression of HMGB1 in PUFA group were less than that in the other two main groups.

CONCLUSIONSLymphatic drainage can alleviate injury of distant organs after intestinal ischemia-reperfusion in rats. ω-3 polyunsaturated fatty acids can increase body resistance to injury and promote recovery.

Animals ; Disease Models, Animal ; Drainage ; Fatty Acids, Omega-3 ; pharmacology ; Intestines ; blood supply ; Liver ; metabolism ; pathology ; Lung ; metabolism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology ; prevention & control

OBJECTIVETo estimate the effect of the lymph duct ligation on systemic inflammatory factors and endotoxins during intestinal ischemia-reperfusion (I/R).

METHODSMale SD rats underwent occlusion of superior mesenteric artery for 60 min followed by reperfusion for 120 min plus lymph duct ligation or not. Forty rats were randomly divided into 4 groups: group A (blank); group B (sham); group C (intestinal I/R); group D (intestinal I/R plus lymph duct ligation). Mesenteric lymph nodes were harvested for standard bacteriologic cultures. The endotoxin, D-lactate, diamine oxidase (DAO), and cytokines in serum were detected.

RESULTSThe rates of bacterial translocation to mesenteric lymph nodes were 40% in group C and 20% in group D. No positive lymph node cultures were encountered in any of group A and B. The serum cytokines (except for sICAM-1) , D-lactate, DAO and endotoxin levels were lower in group D than those in group C (P<0.05), but both were higher than those in group A and B (P<0.05).

CONCLUSIONDuring intestinal I/R injury, blockage the lymph flow from gut into bloodstream decreases the levels of cytokines, and significantly attenuates the increase in intestinal permeability.

Animals ; Disease Models, Animal ; Inflammation ; Intestinal Diseases ; metabolism ; microbiology ; pathology ; Intestines ; blood supply ; pathology ; Ligation ; Lymph Nodes ; pathology ; Lymphatic System ; surgery ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; microbiology ; pathology

Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS). The aim of this study is to determine the effects of ginsenoside Rb1 on liver injury induced by intestinal I/R in rats. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Liver and intestinal histology was observed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) level in serum and malondialdehyde (MDA) level in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-alpha, MDA level and immunohistochemical expression of NF-kappa B and intracellular adhesion molecale-1 (ICAM-1) in liver tissues was assayed. In addition, a western blot analysis of liver NF-kappa B expression was performed. Results indicated intestinal I/R induced intestinal and liver injury, which was characterized by increase of AST and ALT in serum, MDA level in intestine, MPO, TNF-alpha and MDA level and ICAM-1 and NF-kappa B expression in the liver tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated liver injury, decreased MPO, TNF-alpha and MDA level, NF-kappa B and ICAM-1 expression in liver tissues. In conclusion, ginsenoside Rb1 ablated liver injury induced by intestinal I/R by inhibiting NF-kappaB activation.
Alanine Transaminase/blood ; Animals ; Aspartate Aminotransferases/blood ; Biological Markers/metabolism ; Ginsenosides/*pharmacology ; Intercellular Adhesion Molecule-1/metabolism ; Intestines/*blood supply/metabolism/pathology ; Ischemia/metabolism/pathology ; Liver/enzymology/pathology ; Liver Diseases/etiology/*pathology ; Male ; Malondialdehyde/metabolism ; NF-kappa B/*antagonists & inhibitors/metabolism ; Peroxidase/metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury/complications/*pathology ; Tumor Necrosis Factor-alpha/metabolism

AIMTo study the influence of astragalus and zinc sulfate on the viscosity in erythrocyte membrane during intestinal I/R and their mechanism of action.

METHODSModels of rabbits intestinal I/R injury were made. The effect of astragalus and zinc sulfate on the viscosity and malondialdehyde (MDA) in erythrocyte membrane, superoxide dismutase (SOD) in erythrocyte, oxidase (XO) in plasma and MDA tissues homogenate were observed.

RESULTSThe administration of astragalus and zinc sulfate decreased viscosity and MDA and XO, prevented the reduction of SOD, and alleviated I/R injury.

CONCLUSIONLipid peroxidation injury of the erythrocyte membrane was one of the pathogenesis of I/R injury, and astragalus and the zinc sulfate possessed effects of anti-lipid peroxide, stabilized erythrocyte membrane, increased red blood cell deform ability and raised microcircular perfusion.

Animals ; Astragalus Plant ; Blood Viscosity ; Drugs, Chinese Herbal ; pharmacology ; Erythrocyte Membrane ; drug effects ; Female ; Intestines ; blood supply ; pathology ; Lipid Peroxidation ; Male ; Malondialdehyde ; analysis ; Oxidoreductases ; analysis ; Rabbits ; Reperfusion Injury ; metabolism ; pathology ; Superoxide Dismutase ; analysis ; Zinc Sulfate ; pharmacology

The present study aimed to investigate the change of cytochrome c in postconditioning-attenuated ischemia-reperfusion (I/R)-induced mucosal apoptosis in rat intestine compared with ischemic preconditioning (IPC). Using rat model of intestine I/R injury, male Sprague-Dawley rats weighing 220-250 g were divided into 4 groups which were Sham operation group, I/R group, IPC group and ischemic postconditioning (IPOST) group. In these groups, I/R procedure was performed by the occlusion of the superior mesenteric artery (SMA) for 45 min followed by reperfusion for 1 h. In Sham group, there was no intervention. In IPC group, SMA was occluded for 5 min and reperfused for 5 min, for two cycles, before the prolonged occlusion. In IPOST group, three cycles of 30-s reperfusion and 30-s reocclusion were preceded at the start of reperfusion. After the reperfusion, the small intestines were sampled for experimental detection. Intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy. Expressions of cytochrome c and caspase-3 proteins were detected using Western-blot method. The apoptosis of intestinal mucosal cells was determined with agarose gel electrophoresis and deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling (TUNEL) technique. Compared with I/R group, the mitochondrial membrane potentials and the expressions of cytochrome c protein were significantly increased, while the expressions of caspase-3 and the apoptotic rates were decreased in IPOST and IPC groups (P<0.05). There were no significant differences between IPOST and IPC groups (P>0.05). These data provide substantial evidence that IPOST attenuates I/R-induced mucosal apoptosis by reducing the release of cytochrome c from mitochondria in the rat small intestine.
Animals ; Apoptosis ; physiology ; Cytochromes c ; metabolism ; Intestinal Mucosa ; metabolism ; pathology ; Intestines ; blood supply ; Ischemic Postconditioning ; methods ; Male ; Membrane Potential, Mitochondrial ; Mitochondria ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control

OBJECTIVETo investigate cardiac function impairment and myocardial injury in rats with intestinal ischemia-reperfusion and the protective effect of cromolyn sodium.

METHODSThirty-two SD rats were randomized into 4 groups (n=8), namely the sham operation group, model group, 50 mg/kg cromolyn sodium group, and 25 mg/kg cromolyn sodium group. Intestinal damage was induced by clamping the superior mesenteric artery for 45 min followed by reperfusion for 60 min. Cromolyn Sodium was administrated intaperitoneally 15 min before reperfusion. The heart rate (HR), left ventricle pressure (LVSP), and the maximal/minimum rate of LVSP (+dp/dt(max), -dp/dt(max)) were sacrificed immediately before ischemia (baseline, T(0)), at 15 min (T(1)), 30 min (T(2)), 45 min (T(3)) of ischemia, and at 3 min (T(4)), 5 min (T(5)), 10 min (T(6)), 15 min (T(7)), 45 min (T(8)), 60 min (T(9)) of reperfusion. At the end of the experiment, the rats were executed and the hearts were immediately removed for observation of the pathological changes and determination of MDA contents and SOD activity.

RESULTSCompared with the baseline T(0), the HR, +dp/dt(max), -dp/dt(max) and the LVSP were decreased significantly at T(8) and T(9) in the model group and the two cromolyn sodium groups (P<0.05). Compared with the sham operation group, these indices were also significantly decreased at T(8) and T(9) in the model group and the two cromolyn sodium groups, but the model group had significantly lower levels for these indices at T(8) and T(9) than the two cromolyn sodium groups (P<0.05). The score of myocardial injury in the model group and the two cromolyn sodium groups were significantly higher than that of group A, and 50 mg/kg cromolyn sodium group had lower score than the model group (P<0.05). The rats in the model group had significantly higher MDA levels than those in the sham operation group and the 50 mg/kg cromolyn sodium group. SOD activities in the model group and 25 mg/kg cromolyn sodium group was lower than that in the sham operation group (P<0.05), but 50 mg/kg cromolyn sodium group had significantly higher SOD activities than the model group (P<0.05).

CONCLUSIONCromolyn sodium can protect the myocardium against intestal ischemia-reperfusion injury and improve the cardiac function.

Animals ; Cardiotonic Agents ; pharmacology ; Cromolyn Sodium ; pharmacology ; Female ; Heart ; drug effects ; physiopathology ; Heart Rate ; drug effects ; Intestines ; blood supply ; Male ; Malondialdehyde ; blood ; metabolism ; Myocardium ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; blood ; prevention & control ; Superoxide Dismutase ; blood ; metabolism ; Time Factors