epiglucan and Reperfusion-Injury

Ischemia-reperfusion injury has been one of the culprits of tissue injury and flap loss after island flap transpositions. Thus, significant research has been undertaken to study how to prevent or decrease the spread of ischemia-reperfusion injury. Preventive effects of β-glucan on ischemia-reperfusion injury in the kidney, lung, and small intestine have previously been reported. In this study, we present the ameliorating effects of β-glucan on ischemia-reperfusion injury using the epigastric artery island-flap in rats.. Thirty Wistar-Albino rats were equally divided into three groups: sham, experimental model, and treatment groups. In the sham group, an island flap was elevated and sutured back to the original position without any ischemia. In the experimental model group, the same-sized flap was elevated and sutured back with 8 h of ischemia and consequent 12 h of reperfusion. In the treatment group, 50 mg per kilogram β-glucan was administered to the rats using an orogastric tube for 10 d before the experiment. The same-sized flap is elevated and sutured back to its original position with 8 h of ischemia and 12 h of consequent reperfusion in the treatment group. Tissue biopsies were taken on the first day of the experimental surgery. Tissue neutrophil aggregation and vascular responses were evaluated by histological examinations. Tissue oxidant and antioxidant enzyme levels are evaluated biochemically after tissue homogenization. Topographic follow-up and evaluation of the flaps were maintained, and photographs were taken on the first and seventh day of the experimental surgery.. Topographic flap survival was significantly better in the β-glucan administered group. The neutrophil number, malondialdehyde, and myeloperoxidase levels were significantly lower while glutathione peroxidase and superoxide dismutase levels were significantly higher in the β-glucan administered group respective to the experimental model group.. Based on the results of our study, we can conclude that β-glucan is protective against ischemia-reperfusion injury. Our study presents the first experimental evidence of such an effect on skin island flaps.

Topics: Animals; beta-Glucans; Drug Evaluation, Preclinical; Epigastric Arteries; Free Tissue Flaps; Male; Neutrophil Infiltration; Oxidoreductases; Rats, Wistar; Reperfusion Injury; Tissue Survival

Ischemia-reperfusion injury is one of the leading causes of acute renal failure which is a common clinical event leading to development of chronic kidney disease and a high mortality; especially in elderly people. β-glucans are glucose polymer groups with free-radical scavenger, macrophage activator, and immune defense inducer functions. We designed this study to determine the possible protective effects of β-glucan against renal ischemia-reperfusion injury comparatively in young and aged rats.. Rats were assigned to the following groups: Young and aged sham, young and aged ischemia-reperfusion, young and aged β-glucan, young and aged ischemia-reperfusion+β-glucan. At the end of the experiment, following collection of blood samples, rats were sacrificed and kidneys were removed for histopathological and biochemical examination.. Mean tissue histopathological damage scores of young β-glucan group was lower than that of young ischemia-reperfusion group, and of aged β-glucan group was lower than that of aged ischemia-reperfusion group. Urea and creatinine levels of young and aged of sham group and β-glucan administered groups were all lower than those of ischemia-reperfusion and β-glucan+ischemia-reperfusion groups. Oxidative stress indexes of ischemia-reperfusion groups were increased however ; oxidative stress indexes of β-glucan administered to young and aged rats were lower than those of ischemia-reperfusion groups.. We conclude that β-glucan is effective to protect kidneys from ischemia-reperfusion-induced oxidative damage, especially in young rats (Fig. 6, Ref. 45).

Topics: Acute Kidney Injury; Age Factors; Animals; beta-Glucans; Free Radical Scavengers; Ischemia; Kidney; Kidney Failure, Chronic; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reperfusion Injury

Ischemia/reperfusion (IR) injury (IRI) in liver transplant patients may negatively affect graft function. Although β-glucan protects kidneys against IRI, its effect on the liver is unknown. This study sought to investigate β-glucan effects on oxidative damage to the liver after IRI in rats.. Thirty-two rats were randomly divided into 4 experimental groups n = 8 in each group: sham, IR, β-glucan and IR + β-glucan. β-Glucan (50 mg.kg(-1) . day(-1)) was orally administered for 10 days to rats in the β-glucan and IR + β-glucan groups. The rats in the IR and IR + β-glucan groups were subjected to ischemia and reperfusion (IR) for 60 minutes each. All rats were killed on day 11 to evaluate histological changes as well as tissue levels of oxidants and antioxidants.. Malondialdehyde (MDA) levels were significantly higher in the IR than the sham group (P = .001). MDA level was significantly higher in the IR group than in the IR + β-glucan group (P = .001). The levels of tissue antioxidant markers (superoxide dismutase [SOD], glutathione-peroxidase [GPx], and catalase [CAT]) were significantly lower in the IR group than in the sham group (P < .05). SOD and GPx levels did not differ significantly between the IR and IR + β-glucan groups. CAT activity was significantly higher in the IR than the IR + β-glucan group (P = .001). Histological tissue damage was reduced in the IR + β-glucan than the IR group.. Liver IRI is an inevitable problem during liver surgery. Our results suggested that β-glucan pretreatment suppressed oxidative stress and increased antioxidant levels in an rat model of liver IRI.

Topics: Administration, Oral; Animals; Antioxidants; beta-Glucans; Catalase; Disease Models, Animal; Glutathione Peroxidase; Liver; Male; Malondialdehyde; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase

Aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute lung injury following abdominal aortic surgery. The aim of our study was to examine the effect of β-glucan on lung injury induced by abdominal aortic IR in rats.. Thirty-two Wistar-albino rats were randomized into four groups (eight per group) as follows: the control group (sham laparotomy), aortic IR (120 min ischemia and 120 min reperfusion), aortic IR + β-glucan (β-glucan 50 mg/kg/d for 10 d was administered orally before IR), and control + β-glucan. Lung tissue samples were obtained for biochemical analysis. Protein concentrations in bronchoalveolar lavage fluid and lung wet/dry weight ratios were measured. Histologic evaluation of the rat lung tissues was also performed.. Aortic IR significantly increased the levels of MDA, superoxide dismutase, catalase, and myeloperoxidase (P < 0.05 versus control).Whereas, β-glucan significantly decreased the lung tissue levels of MDA, superoxide dismutase, catalase, myeloperoxidase, (P < 0.05 versus aortic IR), and protein concentration in bronchoalveolar lavage fluid as well as wet/dry lung weight ratio. Histologic evaluation showed that β-glucan attenuated the morphological changes associated with lung injury.. The results of this study indicate that β-glucan attenuates lung injury induced by aortic IR in rats. We propose that this protective effect of β-glucan is due to (1) reduced systemic inflammatory response, (2) reduced oxidative stress and lipid peroxidation in the lung tissue, (3) reduced pulmonary microvascular leakage, and (4) inhibition of leukocyte infiltration into the lung tissue.

Topics: Animals; Aorta, Abdominal; beta-Glucans; Catalase; Female; Lung; Lung Injury; Male; Malondialdehyde; Peroxidase; Rats; Rats, Wistar; Reperfusion Injury; Superoxide Dismutase

Ischemia-reperfusion (I/R) injury is one of the leading causes of acute renal failure. Beta-(1-->3)-glucans are glucose polymers with a variety of stimulatory effects on the immune system. We designed this study to determine the possible protective effect of the orally administered soluble beta-glucan against I/R injury.. 30 rats were randomly divided into 5 experimental groups (control, sham operated, beta-glucan, I/R and I/R+beta-glucan groups, n = 6 each). Beta-glucan was administered orally to 6 rats of the beta-glucan and I/R+beta-glucan groups. The rats were subjected to bilateral renal ischemia followed by reperfusion in the I/R and I/R+beta-glucan groups. All of the rats were then sacrificed and kidney function tests, serum and tissue oxidants and antioxidants were evaluated.. The serum urea and cystatin C levels were significantly higher in the I/R group compared to the I/R+beta-glucan group (p < 0.01). The serum and tissue antioxidant markers (SOD, GSH-Px) were significantly lower in the I/R group than the I/R+beta-glucan group (p < 0.01). The serum oxidant markers (NO and PC) were significantly higher in the I/R group than the I/R+beta-glucan group (p < 0.01).. Based on the present data, we conclude that increased antioxidants and decreased oxidants modulated by beta-glucan attenuated the renal I/R injury.

Topics: Administration, Oral; Animals; Antioxidants; beta-Glucans; Cystatin C; Cystatins; Glutathione; Kidney; Kidney Diseases; Male; Oxidative Stress; Random Allocation; Rats; Rats, Wistar; Reperfusion Injury; Urea

N-acetylcysteine, beta-glucan, and coenzyme Q(10) were shown to have antioxidant and anti-inflammatory effects on reperfusion injury. The aim of our study was to determine and evaluate the effects of these agents on ischemia reperfusion injury of limb.. Forty-four New Zealand white rabbits, all female, weighing between 2.3 to 4.2 (mean 3.8) kg, were used in the study. Four study groups were arranged of 11 animals each, by randomization. The first group was the control group (Group C), the other groups were the Group Q, which was medicated with coenzyme Q10, the Group betaG, which was medicated with beta-glucan, and the Group N, medicated with N-acetylcysteine. After baseline measurements, for the ischemia-reperfusion experiments, common iliac artery was clamped and collateral flow was occluded by a rubber arterial tourniquet wrapped around the thigh at the proximal third of the leg. After 60 min of transient ischemic period, the limb was perfused for 180 min. After perfusion, biopsy was taken from the adductor magnus muscle. Second blood sampling was done after reperfusion period. Blood and tissue analysis were done and evaluated statistically.. Baseline and post-reperfusion levels of glutathione peroxidase (GPx), super oxide dismutase (SOD), malonyldialdehyde (MDA), and nitric oxide (NO) changed significantly. While MDA levels increased in the control group, it decreased in the other study groups. The increase in GPx and SOD levels were significant in all groups except the control group. Levels of NO were found to have decreased in the control group, whereas it had increased in the other groups.. Antioxidant medication may help lowering limb ischemia reperfusion injury. All mentioned medications in our study are shown to be able to have an effective role for preventing ischemia reperfusion injury to some extent through their antioxidant properties.

Topics: Acetylcysteine; Animals; Antioxidants; beta-Glucans; Coenzymes; Cytoprotection; Female; Glutathione Peroxidase; Hindlimb; Malondialdehyde; Muscle, Skeletal; Nitric Oxide; Rabbits; Reperfusion Injury; Superoxide Dismutase; Ubiquinone

Pressure ulcers (PU) cause morphological and functional alterations in the skin and visceral organs. In this study we investigated the role of oxidative damage in PUs and the probable beneficial effect of beta-glucan treatment against this damage. beta-glucan is known to have immunomodulatory effects. Experiments were carried on Wistar albino rats. PU was induced by applying magnets over steel plates that were implanted under the skin, to compress the skin and cause ischemia where removing the magnets cause reperfusion of the tissue. Within the first 12 h, rats were subjected to 5 cycles of ischemia/reperfusion (I/R), followed by 12 h ischemia. This protocol was repeated for 3 days. In treatment groups, twice a day during reperfusion periods, beta-glucan was either applied locally (25 mg/kg) as an ointment on skin, or administered orally (50 mg/kg) as a gavage. At the end of the experimental periods, tissue samples (skin, liver, kidney, lung, stomach, and ileum) were taken for the measurement of malondialdehyde (MDA)--an index of lipid peroxidation--and glutathione (GSH)--a key antioxidant--levels. Neutrophil infiltration was evaluated by the measurement of tissue myeloperoxidase activity, while collagen contents were measured for the evaluation of tissue fibrosis. Skin tissues were also examined microscopically. Liver and kidney functions were assayed in serum samples. Local treatment with beta-glucan inhibited the increase in MDA and MPO levels and the decrease in GSH in the skin induced by PU, but was less efficient in preventing the damage in visceral organs. However, systemic treatment prevented the damage in the visceral organs. Significant increases in creatinine, BUN, ALT, AST, LDH and collagen levels in PU group were prevented by beta-glucan treatment. The light microscopic examination exhibited significant degenerative changes in dermis and epidermis in the PU group. Tissue injury was decreased especially in the locally treated group. Thus, supplementing geriatric and neurologically impaired patients with adjuvant therapy of beta-glucan may have some benefits for successful therapy and improving quality of life.

Topics: Administration, Oral; Administration, Topical; Alanine Transaminase; Animals; Antioxidants; beta-Glucans; Collagen; Female; Gastric Mucosa; Glutathione; Ileum; Kidney; Lung; Male; Malondialdehyde; Neutrophil Infiltration; Oxidative Stress; Peroxidase; Pressure Ulcer; Rats; Rats, Wistar; Reperfusion Injury; Skin; Stomach

To investigate the role of beta-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury.. Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2 mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFalpha, IL-1beta, IL-6, IL-10 were measured by ELISA.. CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFalpha, IL-1beta and, IL-6, compared to I/R untreated animals.. The beta-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria.

Topics: Animals; Bacterial Translocation; beta-Glucans; Colony Count, Microbial; Cytokines; Disease Models, Animal; Escherichia coli; Inflammation Mediators; Intestinal Mucosa; Intestine, Small; Male; Proteoglycans; Rats; Rats, Wistar; Reperfusion Injury; Tumor Necrosis Factor-alpha