• Journal of Veterinary Clinics
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• v.18 no.3
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• pp.257-264
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• 2001

This study was performed to investigate the effects of chitosan-trimer (CT) on the prevention of postoperative adhesion formation in the rate model. All animals divided into PBS (control), 1% CT, 3% CT, and chitin treated group. The mean adhesion score in 1% CT group (1.03$\pm$0.63), 3% CT group (0.64$\pm$0.53) and chitin group (1.67$\pm$0.71) was found to be lower than that in control group (2.07$\pm$0.81). More favorable adhesion prevention was achieved in 3% CT group (0.64$\pm$0.53) in comparison with the control group, 1% CT group, and chitin group without any hemorrhagic complications. A statistically significant difference was observed in adhesion formation between control group and 3% CT group (p<0.001). In control group, 44 of 45 sites (97.7%) formed adhesions between the intestine defects. In contrast, 3% CT was effective in reducing the incidence of adhesion formation to 17 to 45 sites (62.2%) (p<0.05). The locations of adhesions were observed in serosa-serosa (60%), serosa-mesentery (13.3%), serosa-connective tissue of testis (10%), omentum-liver (10%), serosa-omentum (3.3%), serosa-cecum (3.3%), and serosa-incision (0%). On the results of histological analysis, grade of inflammation and fibrosis at the sites of postoperative peritoneal adhesion formation were not significantly different in all groups. But, 3% CT showed the lowest score of inflammation and fibrosis. In 3% CT group, the rate of increase of plasma fibrinogen was significantly lower compared with that in control group from pre-operation to 10 days later (p<0.05). There were no appreciable difference in the CBC, leukocyte differential counts and total protein concentrations among four groups. In conclusion, our data suggested that CT should be effective on reducing adhesion formation in experimental rat models. The results also showed that 3% CT does not adversely affect normal wound healing and healthy recovery after operation.

• Journal of Veterinary Clinics
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• v.20 no.1
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• pp.42-48
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• 2003

This study was performed to compare the effect of hyaluronic acid(HA), vitamin I and their combinations for the prevention of postoperative intraperitioneal adhesion in dogs. Twelve mongrel dogs were divided into four groups; HA- (HA Group), vitamin E 800IU- (E8 Group), HA + vitamin E 800IU- (HA+E8 Group) and HA + vitamin E 1600IU-treated group(HA+E16 Group) with three dogs in each group. After celiotomy, five abrasions of 1$\times$1 cm area were made on the antimesenteric serosal surface of the anterior ileocecum with a No. 10 scalpel blade. The five abrasions and peritoneal cavity were coated with 25 of 0.l% HA. Oral supplements of vitamin E were given from the fifth day before the operation to the fourteenth day after the operation. Hematologic values were evaluated before the operation and on the 1st, 4th, 7th and 14th day after the operation. The locations and scores of adhesion were assessed through the second operation on the 21st day after the first operation. The adhesions were located on serosa to mesentary(43.3%)), serosa to serosa(20%), serosa to omentum(5%) and serosa to parietal peritoneum(1.7%). The incidences of adhesion in HA, E8, HA+E8 and HA+E16 groups were 80%, 100%, 47% and 53%, respectively. The scores of adhesion in HA+E8 group(p < 0.05) were lower than those in other groups. This study showed that the combination of HA and vitamin E 800IU was significantly effective in reducing the intraperitoneal adhesion in dogs.

• Korean Journal of Veterinary Research
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• v.47 no.1
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• pp.19-24
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• 2007

The cause and pathogenesis of inflammatory bowel disease remain unknown and no definitetherapy exists until now. The present study was conducted to investigate the anti-inflammatory effectsof a herbal preparation (HemoHIM) in colitis induced by 30 mg of trinitrobenzene sulfonic acid (TNBS)in rats. Sprague-Dawley rats were divided into 5 groups. Each group was treated with 1 mg ofHemoHIM/ml of drinking water, 4 mg of HemoHIM/ml of drinking water, 50 mg of HemoHIM/kgof body weight (i.p. once every other day) or 10 mg/kg of HemoHIMof body weight (i.p. onceevery other day) from the next day. After 2 weeks, rats were sacrificed and morphologic featuresof colons were examined. Ulceration, adhesion, thickening and dilatation were noticed in the colonicmucosa after TNBS instillation. Intraperitoneal injection of HemoHIM (50 and 100 mg/kg of bodyweight) showed the anti-inflammatory effect on adhesion, thickening, dilatation, ulceration, and theinhibition effect on damage score by 72.7% and 90.9%, respectively. Histologically, the colon of TNBS-treated rat showed inflammatory cell infiltration by polymorphonuclear cells, multiple erosive lesionsignificant improvement in these symptoms. The results obtained suggest marked anti-inflamatoryactivity of the HemoHIM at the dose levels examined.

• Journal of Trauma and Injury
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• v.25 no.2
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• pp.63-66
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• 2012

Resection of the bowel is necessary for the repair of a ventral hernia after recovery from trauma in some cases. In such instances, polyester or polypropylene meshcannot be used due to the possibility of infection; we had to use biological mesh instead. We report a case in which a traumatic hernia was repaired with Permacol (Covidien, Norwalk, CT, USA). A 42-year-old male patient had been injured by a factory machine seven months prior to admission. At that time, he had abdominal wall injury and small bowel perforation. His abdominal wall had been a defect after operation. A CT scan of the abdomen showed that the left abdominal wall, which is lateral to left rectus abdominis muscle had only one muscle layer, an external oblique muscle, and that a previous abdominal incision had a defect along the entire incision. During the exploration, 10 cm of small bowel was removed due to firm adhesion to the previous surgical scar. Permacol mesh was applied and fixed with transfascial fixations and tacks by using the intraperitoneal onlay mesh technique. There were no complications after the surgery and the patient was discharged without any problems.

• Journal of Veterinary Clinics
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• v.26 no.6
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• pp.547-555
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• 2009

This study was performed to determine the minimum dose of Poloxamer/Sodium alginate (PX/SA) mixture on preventing intraperitoneal adhesions to evaluate organ toxicity. Twenty five healthy adult mongrel dogs (weighing 4.68${\pm}$1.67 kg) were divided into five experimental groups composed of five dogs respectively; negative control group (NC, non-treated), positive control group (PC, 2% carboxymethyl chitosan solution treated), and experiment 1 group (E1, 0.25 ml PX/SA mixture of abraded area), experiment 2 group (E2, 0.5 ml PX/SA mixture of abraded area), experiment 3 group (E3, 1.0 ml PX/SA mixture of abraded area). Venous blood specimens were collected from all experimental animals for hematologic and biochemical analysis: WBC, fibrinogen, AST, ALT, ALP, BUN and creatinine. The anti-adhesion effect was evaluated using a serosa abrasion model. The denuded ileum was coated with PX/SA mixture, carboxymethyl chitosan solution or neither. The tensile strength of the adhesion site was evaluated with a tensiometer. For histopathological examination, tissue samples of the liver and kidney were collected from all dogs. According to the results, the frequency and tensile strength values for adhesion separation in PX/SA group were significantly lower than those in negative control group (p < 0.05). In E2 group, the tensile strength was significantly decreased in consideration of PX/SA dose. The values of AST, ALT, ALP, BUN and creatinine of the control and the experimental groups showed no statistical differences. No obvious microscopic differences were noted among tissue sections obtained from all groups. The results suggest that PX/SA mixture may be effective on reducing peritoneal adhesion formation in dog and that 0.5 ml PX/SA mixture of abraded area is most effective dose. Moreover, PX/SA mixture was considered not to have toxicity for the liver and the kidney.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.396-401
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• 2007

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate metter (PM) effect on intercellular. adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in asthma-induced Balb/c and IL-10 knock out (KO) mouse. Mouse was sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After induction of asthma mouse placed in the inhalation chamber and exposed to DEP and PM (10 $mg/m^3$). The evidences of pulmonary inflammation were assessed by immunohistochemical stain and westen blot against ICAM-1 and VCAM-1 in the lung tissue. In the immunohistochemical stain, positive reactions for ICAM-1 and VCAM-1 were much stronger in asthma-induced groups and asthma-induced group with DEP or PM than control groups. Although mild positive reactions were appeared in asthma-induced IL-10 KO mice groups, positive reactions were very strong in the asthma-induced group with DEP or PM. In Western blot, expression of VCAM-1 was increased in asthma-induced group with DEP or PM than asthma-induced groups. In the IL-10 KO mouse, ICAM-1 and VCAM-1 expression were increased in asthma-induced group with DEP or PM than asthma-induced groups. DEP and PM exposure have additive effects on the aggravation of inflammatory signs in the asthma-induced murine model. These results suggest that inhalation of DEP and PM in asthmatic patients may aggravate clinical symptoms.

• Molecules and Cells
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• v.39 no.7
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• pp.557-565
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• 2016

The paired immunoglobulin-like type 2 receptor (PILR) family consists of two functionally opposite members, inhibitory $PILR{\alpha}$ and activating $PILR{\beta}$ receptors. PILRs are widely expressed in various immune cells and interact with their ligands, especially CD99 expressed on activated T cells, to participate in immune responses. Here we investigated whether PILR-derived agonists inhibit ${\beta}1$ integrin activity as ligands for CD99. PILR-derived peptides as well as PILR-Fc fusion proteins prevented cell adhesion to fibronectin through the regulation of ${\beta}1$ integrin activity. Especially, PILRpep3, a representative 3-mer peptide covering the conserved motifs of the PILR extracellular domain, prevented the clustering and activation of ${\beta}1$ integrin by dephosphorylating FAK and vinculin, which are major components of focal adhesion. In addition, PILRpep3 inhibited transendothelial migration of monocytes as well as endothelial cell tube formation. Furthermore, upon intraperitoneal injection of PILRpep3 into mice with collagen-induced arthritis, the inflammatory response of rheumatoid arthritis was strongly suppressed. Taken together, these results suggest that PILR-derived agonist ligands may prevent the inflammatory reactions of rheumatoid arthritis by activating CD99.

• Archives of Plastic Surgery
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• v.33 no.5
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• pp.621-626
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• 2006

Purpose: Erythropoietin is traditionally known to regulate erythropoiesis, but recently its protective effect against ischemia-reperfusion injury has been studied mainly in cardiovascular and neuronal systems. This study was planned to investigate the effects of recombinant human erythropoietin on ischemia-reperfusion injury in rat TRAM flap model. Methods: Superiorly based TRAM flap was elevated and ischemic insult was given for four hours. Thirty minutes before reperfusion, single dose recombinant human Erythropoietin(5000IU/kg) was injected via intraperitoneal route in the treatment group. At 24 hours postoperatively, systemic neutrophil count, tissue myeloperoxidase activity, malonyldialdehyde amount, nitric oxide content, tissue water content and histologic finding of inflammation was evaluated. On 10 days postoperatively, flap survival rate, angiogenesis and change in hematocrit level was evaluated. Results: Tissue nitric oxide level was significantly higher and myeloperoxidase activity was significantly lower in the treatment group 24 hours after reperfusion. Tissue water content was significantly lower in the treatment group. Perivascular neutrophil infiltration and intravascular adhesion was marked in the control group. Mean flap survival after ten days was 69% in the treatment group, and 47% in the control group, demonstrating a significant difference. Neovascularization in the treatment group also outnumbered the control group. No significant hematocrit rise was noted ten days after erythropoietin administration. Conclusion: Recombinant human Erythropoietin improved flap survival in ischemia-reperfusion injured rat TRAM flaps, at least partially owing to suppressed inflammation, increased nitric oxide, and enhanced angiogenesis.

• IMMUNE NETWORK
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• v.6 no.1
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• pp.13-19
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• 2006

Background: Granulocyte colony stimulating factor (G-CSF) is known as a cytokine central to the hematopoiesis of blood cells and to modulate their cellular functions. Besides granulocytes and their precursors, monocytes/macrophages and endothelial cells are direct target cells of G-CSF action. G-CSF influences immune cells in an anti inflammatory way. Methods: To evaluate whether G-CSF has a potential for preventing or ameliorating diseases characterized by mucosal inflammation, we used a mouse model with trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. To the mice model G-CSF was administrated daily by intraperitoneal injection. Macroscopic evaluation and immunohistochemical analysis of colonic tissues were performed. Results: Re combinant human G-CSF significantly inhibited LPS-induced TNF-${\alpha}$ mRNA expression in THP-1 cells. As for in vivo relevance, G-CSF dramatically reduced the weight loss of mice, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, G-CSF suppressed the expression of tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$, and intercellular adhesion molecule-1 in TNBS colitis. Conclusion: Current results demonstrate that G-CSF may be an effective agent for the treatment of diseases characterized by mucosal inflammation.

• Genomics & Informatics
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• v.2 no.2
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• pp.75-80
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• 2004

In a variety of animal species, the perinatal exposure of experimental animals to the 2,3,7,8-tetrachlorodibenzo­p-dioxin (TCDD) leads to the immune dysfunction, which is more severe and persistent than that caused by adult exposure. We report here the changes of gene expression and the identification of the marker-genes representing the dioxin exposure. The expressions of the transcripts were analyzed using the 11 K oligonucleotide­microarray from the bone marrow cells of male C57BL/6J mice after an intraperitoneal injection of $1{\mu}g$ TCDD/kg body weight at various time intervals: gestational 6.5 day(G6.5), 13.5 day(G13.5), 18.5 day(G18.5), and postnatal 3 (P3W)and 6 week (P6W). The type of self-organizing maps(SOM) representing the specific exposure dioxin could be identified as follows; G6.5D(C14), G13.5D(C0, C5, C10, C18), G18.5D(7): P3W(C2, C21), and P6W(C4, C15, C20). The candidate marker-genes were restricted to the transcripts, which could be consistently expressed greater than $\pm$2-fold in three experiments. The resulting candidates were 85 genes, the characteristics of that were involved in cell physiology and cell functions such as cell proliferation and immune function. We identified the biomarker-genes for dioxin exposure: smc -like 2 from SOM C14 for the dioxin exposure at G6.5D, focal adhesion kinase and 6 other genes from C0, and protein tyrosine phosphatase 4a2 and 3 other genes from C5 for G13.5D, platelet factor 4 from C7 for G18.5D, fos from C2 for P3W.