Protective effect of rhIL-1β on pancreatic islets of alloxan-induced diabetic rats

AIM: To observe the protective effect of rhIL-1β on pancreatic islets of alloxan-induced diabetic rats. METHODS: Protection of rhIL-1β on pancreatic islets of alloxan-induced diabetic rats (n=5) was demonstrated with methods of immunohistochemistry and stereology. The concentration of serum glucose was measured by GOD method and that of serum insulin by RIA. RESULTS: The concentration of serum glucose increased but that of insulin decreased after administration of alloxan (150mg/kg), and the volume density and numerical density of the islets were zero. In rhIL-1β pretreated rats, although the concentration of serum insulin decreased (from 11.9±3.0mIU/L to 6.1±1.6mIU/L,P<0.05), that of glucose was at normal level compared with the control group. As compared with alloxan group, the concentration of serum glucose in rhIL-1β pretreated rats decreased (from 19.4±8.9mmol/L to 12.0±4.0mmol/L, P<0.05) and the volume density increased(0/L to. 1/L, P<0.05). CONCLUSION: rhIL-1β pretreatment may have protective effect on the islets of alloxan-induced diabetic rats.     

Antidiabetic effects of chitooligosaccharides on pancreatic islet cells in streptozotocin-induced diabetic rats

AIM： To investigate the effect of chitooligosaccharides on proliferation of pancreatic islet cells, release of insulin and 2 h plasma glucose in streptozotocin-induced diabetic rats. METHODS： In vitro, the effect of chitooligosaccharides on proliferation of pancreatic islet cells and release of insulin was detected with optical microscopy, colorimetric assay, and radioimmunoassay respectively. In vivo, the general clinical symptoms, 2 h plasma glucose, urine glucose, oral glucose tolerance were examined after sixty days of feeding study to determine the effect of chitooligosaccharides in streptozotocin-induced diabetic rats. RESULTS： Chitooligosaccharides could effectively accelerate the proliferation of pancreatic islet cells. Chitooligosaccharides （100 mg/L） had direct and prominent effect on pancreastic β cells and insulin release from islet cells. All concentrations of chitooligosaccharides could improve the general clinical symptoms of diabetic rats, decrease the 2 h plasma glucose and urine glucose, and normalize the disorders of glucose tolerance. CONCLUSION： Chitooligosaccharides possess various biological activities and can be used in the treatment of diabetes mellitus.     

Fentanyl inhibits glucose-stimulated insulin release from β-cells in rat pancreatic islets

AIM： TO explore the effects of fentanyl on insulin release from freshly isolated rat pancreatic islets in static culture. METHODS： Islets were isolated from the pancreas of mature Sprague Dawley rats by common bile duct intraductal collagenase V digestion and were purified by discontinuous Ficoll density gradient centrifugation. The islets were divided into four groups according to the fentanyl concentration： control group （0 ng/mL）, group I （0.3 ng/mL）, group I （3.0 ng/mL）, and group III （30 ng/mL）. In each group, the islets were co-cultured for 48 h with drugs under static conditions with fentanyl alone, fentanyl ＋ 0.1 μg/mL naloxone or fentanyl ＋ 1.0 μg/mL naloxone. Cell viability was assessed by the MTT assay. Insulin release in response to low and high concentrations （2.8 mmol/L and 16.7 mmol/L, respectively） of glucose was investigated and electron microscopy morphological assessment was performed. RESULTS： Low- and high-glucose-stimulated insulin release in the control group was significantly higher than in groups I and II （62.33 ± 9.67 μIU vs 47.75 ± 8.47 μIU, 39.67 ± 6.18 μIU and 125.5 ± 22.04 μIU vs 96.17 ± 14.17 μIU, 75.17 ± 13.57 μIU, respectively, P 〈 0.01） and was lowest in group III （P 〈 0.01）. After adding 1 μg/mL naloxone, insulin release in groups II and II was not different from the control group. Electron microscopy studies showed that the islets were damaged by 30 ng/ml fentanyl. CONCLUSION： Fentanyl inhibited glucose-stimulated insulin release from rat islets, which could be prevented by naloxone. Higher concentrations of fentanyl significantly damaged β-cells of rat islets.     

Development of Wistar rat model of insulin resistance

AIM: To establish a simplified and reliable animal model of insulin resistance with low cost in Wistar rats. METHODS: Wistar rats were treated with a high fat emulsion by ig for 10 d. Changes of the diets, drinking and body weight were monitored every day and insulin resistance was evaluated by hyperinsulinemic-euglycemic clamp techniques and short insulin tolerance test using capillary blood glucose. Morphologic changes of liver, fat, skeletal muscles, and pancreatic islets were assessed under light microscope. mRNA expressions of GLUT2 and α-glucosidase in small intestine epithelium, GLUT4 in skeletal muscles and Kir6.2 in beta cell of islets were determined by in situ hybridization. RESULTS: KITT was smaller in treated animals (4.5±0.9) than in untreated control Wistar rats (6.8±1.5), and so was glucose injection rate. Both adipocyte hypertrophy and large pancreatic islets were seen in high fat fed rats, but no changes of skeletal muscles and livers were observed. mRNA levels of GLUT2, α-glucosidase in small intestinal epithelium and Kir6.2 mRNA in beta cells of islets increased, whereas that of GLUT4 in skeletal muscles decreased in high fat fed group compared with normal control group. CONCLUSION: An insulin resistance animal model in Wistar rats is established by ig special fat emulsion.     

In vitro effect of exogenous insulin on insulin secretion. Studies with glucose,leucine, arginine,aminophylline and tolbutamide

Summary Using rat pancreatic islets and the perfused rat pancreas, the effect of exogenous insulin on insulin secretion mediated by glucose, leucine, arginine, aminophylline and tolbutamide was studied. (1) In both systems the insulin releasing capacity of glucose was inhibited by exogenous insulin. In the perfused pancreas the inhibition concerned the first and the second phase of insulin release; (2) the EC50 (half-maximal inhibitory effect of insulin on glucose-induced insulin secretion) in islets was 1.2 nM (=160 μU/ml) and 2.8 nM (390 μU/ml) in perfused pancreas; (3) exogenous insulin also inhibited insulin release in response to leucine and arginine in the isolated islet system and in the perfused pancreas; (4) using aminophylline and tolbutamide in combination with glucose, the extent of the inhibitory effect of insulin was in the range of the inhibitory effect when glucose was used alone as stimulator in islets. Data suggest that the insulinogenic action of physiological stimulators including glucose, leucine and arginine is inhibited by exogenous insulin whereas this seems not to be the case when insulin release was stimulated by aminophylline and tolbutamide. Comparing the EC50s, isolated islets seem to be more sensitive to inhibition than the perfused pancreas when glucose was used as stimulator. As far as glucose is concerned the inhibitory effect seems to depend on the extent of its concentration and/or the extent to which the mechanism of insulin release is sensitive to stimulation. The EC50 of the inhibitory effect of exogenous insulin was in the range of dissociation constant of binding of insulin to insulin receptors of islets. Preliminary data on this study have been presented at the 22th Spring Meeting of theDeutsche Pharmakologische Gesellschaft, Mainz, F.R.G., March 10–13, 1981. This study was supported by grants of theDeutsche Forschungsgemeinschaft, Bonn-Bad Godesberg, F.R.G.     

Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats

AIM： To observe the effect of proteasome inhibitor MG-132 on severe acute pancreatitis （SAP） and associated lung injury of rats. METHODS： Male adult SD rats were randomly divided into SAP group, sham-operation group, and MG-132 treatment group. A model of SAP was established by injection of 5% sodium taurocholate into the biliary- pancreatic duct of rats. The MG-132 group was pretreated with 10 mg/kg MG-132 intraperitoneally （ip） 30 min before the induction of pancreatitis. The changes in serum amylase, myeloperoxidase （MPO） activity of pancreatic and pulmonary tissue were measured. The TNF-α level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay （ELISA） kit. Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed. RESULTS： MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-α level, pancreatic and pulmonary MPO activity （P 〈 0.05）. Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity （P 〈 0.05）. CONCLUSION： The proteasome inhibitor MG-132 shows a protective effect on severe acute pancreatitis and associated lung injury of rats.     

白藜芦醇对原代大鼠胰岛葡萄糖刺激的胰岛素分泌的影响

Isolated freshly rat islets were transferred to 24-well plates and incubated with different concentrations of glucose or resveratrol for 1 or 24 h.The results showed that resveratrol dose-dependently inhibited glucose-stimulated insulin secretion from isolated rat islets after 1 h incubation,with 10%,35%,and 80% (P<0.05 or P<0.01) decrease at the concentrations of 1,I0,and 100 μmol/L.10 μmol/L resveratrol decreased the intracellular calcium concentration by 60% (P<0.05).After incubation for 24 h,resveratrol increased palmitatesuppressed insulin secretion to 75% (P<0.01) of control.These results suggest that resveratrol acutely inhibits insulin secretion from primary pancreatic islet via regulating intracellular calcium ion concentration,and in the long run resveratrol may protect β-cells from lipotoxicity.     

白藜芦醇对原代大鼠胰岛葡萄糖刺激的胰岛素分泌的影响

Isolated freshly rat islets were transferred to 24-well plates and incubated with different concentrations of glucose or resveratrol for 1 or 24 h.The results showed that resveratrol dose-dependently inhibited glucose-stimulated insulin secretion from isolated rat islets after 1 h incubation,with 10%,35%,and 80% (P<0.05 or P<0.01) decrease at the concentrations of 1,I0,and 100 μmol/L.10 μmol/L resveratrol decreased the intracellular calcium concentration by 60% (P<0.05).After incubation for 24 h,resveratrol increased palmitatesuppressed insulin secretion to 75% (P<0.01) of control.These results suggest that resveratrol acutely inhibits insulin secretion from primary pancreatic islet via regulating intracellular calcium ion concentration,and in the long run resveratrol may protect β-cells from lipotoxicity.     

Spontaneous diabetes-like syndrome in WBN/Kob rats

Summary Spontaneous hyperglycemia, glycosuria, hypoinsulinemia, and glucose intolerance were observed in some WBN/Kob rats, at about 9 months of age, and in all at the age of 17 months. Females did not present this pathology. Histopathologic examination of the pancreas revealed severe changes in male rats at the age of 3 months. Between 3 and 6 months of age a distinct infiltration of inflammatory cells was found around islets and among adjacent acinar cells. At the same time, marked fibrosis was seen around the pancreatic ducts and blood vessels. With advancing age the fibrous tissue gradually invaded extensive areas of the pancreas where also the islets became involved in fibrotic degeneration. At 17 months of age and later, an obvious decrease in islet number and size (less than 50 μ in diameter) was observed, even in relatively unaffected areas of the organ. Frequent bilateral cataracts began to appear at about 15 months of age. Opacities were first observed in the periphery of the lens, then increased rapidly in intensity and extended centripetally. Nineteen-month-old male rats were hypersensitive to exogenous insulin, but showed no significant decrease in blood glucose level when treated with oral tolbutamide. These results suggest that these rats suffered from a decreased insulinogenic response.     

Small intestinal submucosa improves islet survival and function during in vitro culture

AIM: To evaluate the recovery and function of isolated rat pancreatic islets during in vitro culture with small intestinal submucosa (SIS). METHODS: Pancreatic islets were isolated from Wistar rats by standard surgical procurement followed by intraductal collagenase distension, mechanical dissociation and Euroficoll purification. Purified islets were cultured in plates coated with multilayer SIS (SIS-treated group) or without multilayer SIS (standard cultured group) for 7 and 14 d in standard islet culture media of RPMI 1640. After isolation and culture, islets from both experimental groups were stained with dithizone and counted. Recovery of islets was determined by the ratio of counts after the culture to the yield of islets immediately following islet isolation. Viability of islets after the culture was assessed by the glucose challenge test with tow (2.7 mmol/L) and high glucose (16.7 mmol/L) solution supplemented with 50 mmol/L 3-isobutyl-1-methylxanthine (IBMX) solution. Apoptosis of islet cells after the culture was measured by relative quantification of histone-complexed DNA fragments using ELISA. RESULTS: After 7 or 14 d of in vitro tissue culture, the recovery of islets in SIS-treated group was significantly higher than that cultured in plates without SIS coating. The recovery of islets in SIS-treated group was about twice more than that of in the control group. In SIS-treated group, there was no significant difference in the recovery of islets between short- and long-term periods of culture (95.8±1.0% vs 90.8±1.5%, P>0.05). When incubated with high glucose (16.7 mmol/L) solution, insulin secretion in SIS-treated group showed a higher increase than that in control group after 14 d of culture (20.7±1.1 mU/L vs 11.8±1.1 mU/L, P<0,05). When islets were placed in high glucose solution containing IBMX, stimulated insulin secretion was higher in SIS-treated group than in control group. Calculated stimulation index of SIS-treated group was about 23 times of control group. In addition, the stimulation index of SIS-treated group remained constant regardless of short- and long-term periods of culture (9.5±0.2 vs 10.2±1.2, P>0.05). Much less apoptosis of islet cells occurred in SIS-treated group than in control group after the culture. CONCLUSION: Co-culture of isolated rat islets with native sheet-like SIS might build an extracellular matrix for islets and provide possible biotrophic and growth factors that promote the recovery and subsequent function of islets.     

Protective effects of rhubarb on experimental severe acute pancreatitis

AIM:To investigate the effects of rhubarb on severe acutepancreatitis (SAP) in rats.METHODS:Severe acute pancreatitis was induced by twointraperitoneal injections of cerulein (40 μg/kg body weight)plus 5-h restraint water-immersion stress.Rhubarb (75-150 mg/kg) was orally fed before the first cerulein injection.The degree of pancreatic edema,serum amylase level,local pancreatic blood flow (PBF),and histologicalalterations were investigated.The effects of rhubarb onpancreatic exocrine secretion in this model were evaluatedby comparing with those of somatostatin.RESULTS:In the Cerulein Stress group,severe edemaand diffuse hemorrhage in the pancreas were observed,the pancreatic wet weight (11.60±0.61 g/Kg) and serumamylase (458 490±43 100 U/L) were markedly increased(P<0.01 vs control).In the rhubarb (150 mg/kg) treatedrats,necrosis and polymorphonuclear neutrophil (PMN)infiltration in the pancreas were significantly reduced(P<0.01),and a marked decrease (50%) in serum amylaselevels was also observed (P<0.01).PBF dropped to 38%(93±5 mL/min per 100 g) of the control in the Cerulein Stressgroup and partly recovered in the Cerulein Stress Rhubarb150 mg group (135±12 mL/min per 100 g) (P<0.01).Thepancreatic exocrine function was impaired in the SAP rats.The amylase levels of pancreatic juice were reduced in therats treated with rhubarb or somatostatin,comparing withthat of untreated SAP group.The bicarbonate concentration ofpancreatic juice was markedly elevated only in the rhubarb-treated group (P<0.01).CONCLUSION:Rhubarb can exert protective effects onSAP,probably by inhibiting the inflammation of pancreas,improving pancreatic microcirculation,and altering exocrinesecretion.     

Effect of insulin and metformin on methylation and glycolipid metabolism of peroxisome proliferator-activated receptor γcoactivator-1A of rat offspring with gestational diabetes mellitus

Objective:To discuss the effect of insulin and metformin on amethylation and glycolipid metabolism of peroxisome proliferator-activated receptor γ coactivator-1A(PPARGC1A) of rat offspring with gestational diabetes mellitus(GDM).Methods:A total of 45 pregnant rats received the intraperitoneal injection of streptozotocin to establish the pregnant rat model of GDM.A total of 21 pregnant rats with GDM were randomly divided into three groups,with 7ruts in each group,namely the insulin group,metformin group and control group.Rats in the insulin group received the abdominal subcutaneous injection of 1 mL/kg recombinant insulin glargine at 18:00 every day.Rats in the metformin group received the intragastric infusion of metformin hydrochloride at 18:00 every day,with the first dose of 300 mg/kg.The doses of two groups were adjusted every 3 d to maintain the blood glucose level at 2.65-7.62 mmol/L.Rats in the control group received the intragastric infusion of 1 mL normal saline at 18:00 every day.After the natural delivery of pregnant rats.10 offspring rats were randomly selected from each group.At birth,4 wk and 8 wk after the birth of offspring rats,the weight of offspring rats was measured.The blood glucose level of offspring rats was measured at 4wk and 8 wk,while the level of serum insulin,triglyceride and leptin was measured at 8 wk.Results:The weight of offspring rats at birth in the insulin group and metformin group was significantly lower than the one in the control group(P0.05),and there was no significant difference at 4 wk and 8 wk among three groups(P0.05).The fasting blood glucose and random blood glucose in the insulin group and metformin group at 4 wk and 8 wk were all significantly lower than ones in the control group(P0.05);there was no significant difference between the insulin group and metformin group(P0.05).The expression of PPARGC1 A mRNA in the insulin group and metformin group was significantly higher and the methylation level of PPARGC1 A was significantly lower than the one in the control group(P0.05),but there was no significant difference between the insulin group and metformin group(P0.05).Insulin and leptin at 8 wk in the insulin group and metformin group were significantly higher,while triglyceride was significantly lower than the one in the control group(P0.05);triglyceride level of rats in the insulin group was significantly higher than the one in the metformin group(P0.05).There was no significant difference in insulin and leptin level of offspring rats between the insulin group and metformin group(P0.05).Conclusions:GDM can induce the methylation of PPARGC1 A of offspring rats to reduce the expression of PPARGC1 A mRNA and then cause the disorder of glycolipid metabolism when the offspring rats grow up;the insulin or metformin in the treatment of pregnant rats with GDM can reduce the methylation level of PPARGC1 A and thus improve the abnormal glycolipid metabolism of offspring rats.     

The role of ranitidine infusion on glucose,insulin and C-peptide serum levels induced by oral glucose tolerance test in healthy subjects

Summary In 9 healthy subjects we evaluated the effect of a constant ranitidine infusion (100 mg) on glucose (mg/dl), insulin (μU/ml) and C-peptide (ng/ml) serum levels promoted by oral glucose tolerance test (75 g). Ranitidine significantly increased the area under concentration/time curves for glucose and insulin but not that of C-peptide. Our data indicate that ranitidine does not affect pancreatic insulin release nor peripheral glucose utilization and are consistent with the hypothesis that ranitidine influences the hepatic clearance of glucose and insulin both of which undergo high first-pass liver extraction.     

Tumor necrosis factor α antibody prevents brain damage of rats with acute necrotizing pancreatitis

AIM:To study the protective effects of tumor necrosis factor α(TNFα)antibody on pancreatic encephalopathy in rats.METHODS:One hundred and twenty SD rats were randomlydivided into normal control group,acute necrotizingpancreatitis group and TNFα antibody treated group.Acutehemorrhage necrotizing pancreatitis model in rats wasinduced by retrograde injection of 50g/L sodium taurocholateinto the pancreatobiliary duct.Serum TNFα was detectedand animals were killed 12 h after drug administration.Changes in content of brain water,MDA and SOD as wellas leucocyte adhesion of brain microvessels were measured.RESULTS:In TNFα antibody treated group,serum TNFαlevel was decreased.Content of brain water,MDA and SODas well as leucocyte adhesion were decreased significantlyin comparison with those of acute necrotizing pancreatitisgroup (P<0.05).CONCLUSION:TNFα antibody can alleviate the brain damageof rats with acute hemorrhage necrotizing pancreatitis.     

Insulin is necessary for the hypertrophic effect of cholecystokinin-octapeptide following acute necrotizing experimental pancreatitis

AIM: In previous experiments we have demonstrated that by administering low doses of cholecystokinin-octapeptide (CCK-8), the process of regeneration following L-arginine (Arg)-induced pancreatitis is accelerated. In rats that were also diabetic (induced by streptozotocin, STZ), pancreatic regeneration was not observed. The aim of this study was to deduce whether the administration of exogenous insulin could in fact restore the hypertrophic effect of CCK-8 in diabetic-pancreatitic rats.METHODS: Male Wistar rats were used for the experiments.Diabetes mellitus was induced by administering 60 mg/kg body mass of STZ intraperitoneally (i.p.), then, on d 8, pancreatitis was induced by 200 mg/100 g body mass Argi.p. twice at an interval of 1 h. The animals were injected subcutaneously twice daily (at 7 a.m. and 7 p.m.) with 1 μglkg of CCK-8 and/or 2 IU mixed insulin (300 g/L shortaction and 700 g/L intermediate-action insulin) for 14 d after pancreatitis induction. Following this the animals were killed and the serum amylase, glucose and insulin levels as well as the plasma glucagon levels, the pancreatic mass/body mass ratio (pm/bm), the pancreatic contents of DNA, protein, amylase, lipase and trypsinogen were measured. Pancreatic tissue samples were examined by light microscopy on paraffin-embedded sections.RESULTS: In the diabetic-pancreatitic rats treatment with insulin and CCK-8 significantly elevated pw/bm and the pancreatic contents of protein, amylase and lipase vs the rats receiving only CCK-8 treatment. CCK-8 administered in combination with insulin also elevated the number of acinar cells with mitotic activities, whereas CCK-8 alone had no effect on laboratory parameters or the mitotic activities in diabetic-pancreatitic rats.CONCLUSION: Despite the hypertrophic effect of CCK-8 being absent following acute pancreatitis in diabetic-rats,the simultaneous administration of exogenous insulin restored this effect. Our results clearly demonstrate that insulin is necessary for the hypertrophic effect of low-doses of CCK-8 following acute pancreatitis.     

Insulin is necessary for the hypertrophic effect of cholecystokinin-octapeptide following acute necrotizing experimental pancreatitis

AIM:In previous experiments we have demonstrated thatby administering low doses of cholecystokinin-octapeptide(CCK-8),the process of regeneration following L-arginine(Arg)-induced pancreatitis is accelerated.In rats that werealso diabetic(induced by streptozotocin,STZ),pancreaticregeneration was not observed.The aim of this study wasto deduce whether the administration of exogenous insulincould in fact restore the hypertrophic effect of CCK-8 indiabetic-pancreatitic rats.METHODS:Male Wistar rats were used for the experiments.Diabetes mellitus was induced by administering 60mg/kgbody mass of STZ intraperitoneally(i.p.),then,on d 8,pancreatitis was induced by 200mg/100 g body mass Argi.p.twice at an interval of 1 h.The animals were injectedsubcutaneously twice daily(at 7 a.m.and 7 p.m.)with1 μg/kg of CCK-8 and/or 2 IU mixed insulin(300g/L short-action and 700g/L intermediate-action insulin) for 14 dafter pancreatitis induction.Following this the animals werekilled and the serum amylase,glucose and insulin levelsas well as the plasma glucagon levels,the pancreaticmass/body mass ratio(pm/bm),the pancreatic contentsof DNA,protein,amylase,lipase and trypsinogen weremeasured.Pancreatic tissue samples were examined bylight microscopy on paraffin-embedded sections.RESULTS:In the diabetic-pancreatitic rats treatment withinsulin and CCK-8 significantly elevated pw/bm and thepancreatic contents of protein,amylase and lipase vs therats receiving only CCK-8 treatment.CCK-8 administeredin combination with insulin also elevated the number ofacinar cells with mitotic activities,whereas CCK-8 alonehad no effect on laboratory parameters or the mitoticactivities in diabetic-pancreatitic rats.CONCLUSION:Despite the hypertrophic effect of CCK-8being absent following acute pancreatitis in diabetic-rats,the simultaneous administration of exogenous insulin restored this effect.Our results clearly demonstrate thatinsulin is necessary for the hypertrophic effect of low-dosesof CCK-8 following acute pancreatitis.     

Evaluation of protective effect of cactus pear seed oil(Opuntia ficusincida L. MILL.) against alloxan-induced diabetes in mice

Objective: To evaluate the in vitro antioxidant power of cactus pear seed oil [Opuntia ficusincida L. MILL.(CPSO)] and its protective effect against chemically induced diabetes mellitus in mice. Methods: The in vitro antioxidant effect of CPSO was evaluated using 2,2-diphenyl-1-picrylhydrazyl(DPPH) scavenging assay. The preventive effect was conducted on Swiss albino mice treated with CPSO(2 m L/kg, per os), before and after a single intraperitoneal alloxan administration(100 mg/kg). Survival rate, body weight and fasting blood glucose were measured and histopathological analysis of pancreas was performed to evaluate alloxaninduced tissue injuries. Results: CPSO exhibited an antioxidant effect in DPPH scavenging assay. Moreover, the administration of CPSO(2 m L/kg) significantly attenuated alloxaninduced death and hyperglycemia(P0.001) in treated mice. Morphometric study of pancreas revealed that CPSO significantly protected islets of langerhans against alloxan induced-tissue alterations. Conclusions: Based on theses results, CPSO can prevent alloxan-induced-diabetes by quenching free radicals produced by alloxan and inhibiting tissue injuries in pancreatic β-cells.     

Antioxidant activity of chito-oligosaccharides on pancreatic islet cells in streptozotocin-induced diabetes in rats

AIM： To investigate the antioxidant activity of chitooligosaccharides （COSs） on pancreatic islet cells in diabetic rats induced by streptozotocin.
METHODS： The antioxidant effect of COSs on pancreatic islet cells was detected under optical microscopy and with colorimetric assay and gel electrophoresis. The activities of glutathione peroxidase and superoxide dismutase, total antioxidant capacity, and content of malondialdehyde in serum and tissue slices of pancreas were examined after 60 d to determine the effect of COSs in streptozotocin-induced diabetes in rats.
RESULTS： COSs can prohibit the apoptosis of pancreatic islet cells. All concentrations of COSs can improve the capability of total antioxidant capacity and activity of superoxide dismutase and decrease the content of malondialdehyde drastically. Morphological investigation in the pancreas showed that COSs have resulted in the reduction of islets, loss of pancreatic cells, and nuclear pyknosis of pancreatic cells.
CONCLUSION： COSs possess various biological activities and can be used in the treatment of diabetes mellitus.