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BACKGROUND: Porcine pancreatic islet transplantation is a common treatment for diabetes mellitus, but inflammatory reaction and oxidative stress can lead to poor long-term effect. It has been confirmed that transplantation of porcine bone marrow mesenchymal stem cells with islets can improve graft function. However, it has not been reported that porcine bone marrow mesenchymal stem cells regulate the expression of miR-299-5p in islet cells to regulate the function and survival rate of islet β cells. OBJECTIVE: To investigate the effects of bone marrow mesenchymal stem cells in pigs on functional impairment of islet in pig by regulating the JNK/C-Jun pathway through the miR-299-5p/SIAH1 molecular axis. METHODS: Lipopolysaccharide was used to induce functional impairment of porcine islet cells, which were co-cultured with bone marrow mesenchymal stem cells for 24 hours. Interleukin-6, interleukin-1β, tumor necrosis factor-α, reactive oxygen species, superoxide dismutase and insulin levels in islet cells were detected by ELISA. Hoechst 33258 staining was used to observe apoptosis. Annexin V-FITC/PI was used to detect the apoptosis rate of porcine islet cells. Western blotting was used to detect the expression of SIAH1 and proteins associated with JNK/C-Jun pathway. The expression of miRNAs in porcine islet cells was detected by qPCR. The dual-luciferase reporter gene assay verified the targeting relationship between miR-299-5p and SIAH1. RESULTS AND CONCLUSION: (1) Bone marrow mesenchymal stem cells in pigs inhibited the up-regulation of interleukin-6, interleukin-1β, tumor necrosis factor-α, reactive oxygen species and pro-apoptotic effects, and also inhibited the down-regulation of superoxide dismutase and insulin secretion induced by lipopolysaccharide. (2) Bone marrow mesenchymal stem cells of pigs significantly upregulated miR-299-5p expression. miR-299-5p inhibited activation of the JNK/C-Jun pathway by down-regulating SIAH1 expression. (3) Results indicate that bone marrow mesenchymal stem cells of pigs inhibit the activation of the JNK/C-Jun pathway, inhibit the inflammatory response, oxidative stress and apoptosis of islet cells in pigs, and promote the secretion of insulin by regulating the miR-299-5p/SIAH1 axis, hereby improving the functional damage of porcine islet cells.
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Objective To explore the possible mechanism of Jianyi Recipe for improving the function of islet cells from the aspects of synthesis,secretion and inactivation of glucagon-like peptide-1 (GLP-1).Methods The diabetic rat model was established by feeding with high-lipid food combined with injection of streptozotocin (STZ).The rats were randomly divided into model group,Jianyi Recipe group,and normal group.The treatment for the rats lasted for 4 weeks.The blood glucose level was detected by the rapid blood glucose meter.The plasma levels of GLP-1 and insulin were detected by Luminex liquid phase protein chip technology.Pancreatic duodenal homeobox-1 (PDX-1) mRNA expression level was detected by quantitative real-time fluorescence polymerase chain reaction (PCR).The level of GLP-1 in ileum L cells was detected by immunohistochemistry,and dipeptidyl peptidase Ⅳ (DPP-Ⅳ)level was detected by enzyme-linked immunosorbent assay.Results Jianyi Recipe could decrease the levels of fasting blood glucose and postprandial glucose (P ＜ 0.05),promote the secretion of insulin (P ＜ 0.05),and increase PDX-1 mRNA expression level in the pancreas of the diabetic rats.Compared with the model group,plasma GLP-1 level,and ileal GLP-1 positive expression area and integrated optical density were increased (P ＜ 0.05) in Jianyi Recipe group,while the differences of serum DPP-Ⅳ levels were insignificant between the two groups (P＞ 0.05).Conclusion Jianyi Recipe maybe regulate the synthesis and secretion of GLP-1 to promote PDX-1 gene expression and insulin secretion,so as to reduce blood glucose in diabetic rats.
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AIM: To observe the anti-apoptosis effect of liraglutide on the islet through microRNA-375 (miR-375) for providing additional pharmacodynamic evidence for its clinical application.METHODS: For in vivo study, C57BL/KsJ-db/m mice aged 8 weeks served as normal control group.A total of 40 male genetically diabetic C57BL/KsJ-db/db mice at the same age were randomly divided into diabetic control group (the db/db mice were injected subcutaneous-ly with equivalent amount of saline) and liraglutide group (the db/db mice were injected subcutaneously with liraglutide at dose of 300 μg? kg-1? d-1 ).After 8 weeks of administration, body weight (BW) was measured and blood was collected for detection of fasting blood glucose (FBG), fasting blood insulin (FINS), triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C).Before sacrifice, intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) were conducted.The histopathological features in the islet tissue were examined with HE staining.The apoptosis in the islet tissue was detected by TUNEL staining.The protein levels of caspase-3, Bcl-2 and Bax were deter-mined by Western blot.The level of miR-375 in the islet tissue was detected by qPCR.For in vitro study, the MIN-6 cells were cultured and divided into control group (incubated with equivalent amount of solvent), miR-375 mimic group and miR-375 mimic +liraglutide group.The cell viability was examined by MTT assay.The protein levels of caspase-3, Bcl-2 and Bax were detected by Western blot.RESULTS: In the in vivo study, compared with control group, the levels of BW, FBG, FINS, TC, TG and LDL-C were decreased significantly in liraglutide group.The islet apoptosis was reduced by the administration of liraglutide.The expression of Bcl-2 was up-regulated significantly, while the protein levels of caspase-3 and Bax were down-regulated significantly in liraglutide group.The level of miR-375 was decreased significantly.In the in vitro study, the cell viability was decreased in miR-375 mimic group and increased in miR-375 mimic +liraglutide group. Moreover, the expression of Bcl-2 was decreased and the protein levels of caspase-3 and Bax were increased with the incu-bation of miR-375 mimic, while the expression of Bcl-2 was increased and the protein levels of caspase-3 and Bax were de-creased with the co-incubation of miR-375 mimic and liraglutide.CONCLUSION: Liraglutide attenuates islet apotosis, and the mechanism may be associated with its effects of reducing the elevated level of miR-375 in islet tissues.
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Objective To isolate and culture human adipose-derived stem cells (hADSCs),investigate the influence of hADSCs on the cellular morphology,survival rate,and function of human islet cells under the in vitro non-contact co-culture conditions,and explore its mechanism.Method hADSCs were isolated by collagenase digestion method,then cultured,and identified by morphology,immunofluorescence and multi-directional differentiation.Adult islet cells were separated and purified by Liberase enzyme and Ficoll 400,then divided into co-culture group and individual group.The cellular growth morphology of islet cells was observed by inverted phase contrast microscope.The survival rate of islet cells,insulin secretory volume,insulin stimulation index and concentration of growth factor in the supernatant were compared between the two groups.Result hADSCs of the third generation showed uniform long spindle fibrocyte-like morphology,and had multi-directional differentiational potentials of osteogenesis and adipogenesis.Immunofluorescence test of surface antigens on hADSCs revealed CD44 + and CD49d +,CD31-,CD34-and CD106-.After 14-day culture,the islet cellular morphology in co-culture group was more intact than that in individual group.The survival rate of islet cells in co-culture group was (82.83 + 2.32) ％,and that in individual group was (53.00 + 2.82) ％ (P＜0.01).Insulin secretory volumes were (23.66 + 2.11) and (7.82 +1.09) mU/L respectively in co-culture group and individual group under high glucose concentration,and 13.22 + 0.77 and 6.40 + 0.44 mU/L respectively under low glucose concentration (P＜0.01 for all).Insulin stimulation index was decreased from 1.67 + 0.10 (at 3rd day) to 1.77 + 0.13 (at 14th day) in co-culture group,and from (1.67 + 0.10) (at 3rd day) to (1.77 + 0.13) (at 14th day) in individual group (P＜0.01).After 14-day culture,the concentrations of HGF,TGF-β,VEGF and bFGF in the supernatant were higher in co-culture group than in individual group (P＜0.01).Conclusion hADSCs were isolated and cultured successfully from adult adipose tissue.They could increase the survival rate and improve the function of islet cells when co-culture with the adult islet cells in vitro through secreting HGF,TGF-β,VEGF and b-FGF.
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[ ABSTRACT] AIM:To investigate whether the increase in PTEN expression is related to apoptosis, and whether it is regulated by reactive oxygen species( ROS) .METHODS: The rat islet cells were divided into constant low glucose group ( group L) , constant high glucose group ( group H) , glucose fluctuation group ( group F) , low glucose after high glucose group (group HL) and low glucose after fluctuation group (group FL).The ROS level, apoptotic rate, intracellu-lar calcium, insulin release and PTEN protein expression were analyzed.RESULTS:Compared with groups H and L, the insulin secretion decreased, and intracellular calcium, ROS level, PTEN protein expression and apoptotic rate increased in group F ( P<0.05) .Compared with group H, the intracellular calcium, ROS level, PTEN protein expression and apoptot-ic rate in group HL decreased, but were still higher than those in group L (P<0.05).Compared with group F, the intra-cellular calcium, ROS level, PTEN protein expression and apoptotic rate in group FL decreased, but were still higher than those in group L (P<0.05).CONCLUSION:Glucose fluctuation can cause the apoptosis of islet cells more easily than constant high glucose.This may be related to the change of intracellular calcium and increase in oxidative stress which pro-motes PTEN expression.The recovery of glucose level to some extent relieves oxidative stress, decrease PTEN expression and reduce cell damage.
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Objective:To investigate the effect of TNF-αand IFN-γon NIT-1 cells apoptosis and the apoptosis mechan-ism.Methods:NIT-1 cells were exposed to a combination of TNF-αand IFN-γtreatment.The viability of NIT-1 cells was assessed via MTT assay.The morphological changes of the cells and nuclei were observed under the inverted or confocal laser scanning microscope with Hoechst 33258 staining.The activation of Caspase-8,-3 and PARP was detected by Western blot.Results:TNF-αand IFN-γsig-nificantly inhibited NIT-1 cells viability, promoted cells apoptosis, induced the activation of Caspase-8,-3 and PARP cleavage.Conclusion:TNF-αcombined with IFN-γtreatment induced the apoptosis of NIT-1 cells through death receptor pathway.
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The pancreatic tissues from patients with islet cell hyperplasia,insulinoma,and pancreatic adenocarcinoma,as well as normal pancreatic tissues were embedded with paraffin,serial sections were cut and mounted on glass slides.Immunohistochemical staining was carried out with N-myc down-stream regulated gene 2 (Ndrg2) monoclonal antibody by means of ABC method,and Western blotting was carried out to detect the expression and distribution of Ndrg2.The results showed that Ndrg2 positive immunoreactivity was mainly localized in the cytoplasm of islet cell,being similar to the localization of insulin positive immunoreactivity.The number and volume of pancreatic islets were increased in the patients with islet cell hyperplasia,and Ndrg2 expression was also increased.Western blotting results showed that the expression of Ndrg2 in the pancreas of patients with islet cell hyperplasia was increased compared with normal group.The above results suggest that Ndrg2 may play an important role in performing physiological function of islet cells.
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BACKGROUND:Drug treatment is the main method for the treatment of diabetes currently, but the development of the disease and occurrence of related complications are the chal enges to the effect of drugs. OBJECTIVE:To investigate the effect and feasibility of co-transplantation of bone marrow mesenchymal stem cells and islet cells for the treatment of diabetes. METHODS:The rat bone marrow mesenchymal stem cells were separated and purified, and cultured in vitro to establish the diabetes models. The rat diabetes models were injected with bone marrow mesenchymal stem cells, co-cultured mixture of bone marrow mesenchymal stem cells and islet cells, and normal saline or phosphate buffer (control). The effect of transplantation was evaluated through observing the blood glucose levels, insulin secretion, and pathological changes of pancreatic tissue in the rat diabetes models. RESUTLS AND CONCLUSION:In the diabetes rats treated with bone marrow mesenchymal stem cel transplantation, the C-peptide levels were significantly increased after transplantation, while the blood glucose levels were significantly decreased, but not lower than the normal level, and the blood glucose levels were increased again with the time prolonging. In the diabetes rats treated with co-transplantation of bone marrow mesenchymal stem cells and islet cells, the blood glucose levels were decreased significantly and lower than the normal level which was maintained in a certain time, and the decreasing degree was larger than that in the rats treated with simple bone marrow mesenchymal stem cel transplantation. Co-transplantation of bone marrow mesenchymal stem cells and islet cells is feasible for the treatment of diabetes with a certain effect.
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The Possible Revival of atrophied islet cells of the pancreas by Vernonia amygdalina in alloxan-induced diabetic rats was evaluated. Twenty rats were divided into five groups (1, 2, 3, 4 and 5) of four rats each. Group 1 rats were given only feed and distilled water (normal control) throughout the period of the experiment. Group 3, 4 and 5 rats were pretreated with 250mg/kg body weight of the extract for 7, 14 and 21 days respectively. Diabetes was induced in rats in group 2, 3, 4 and 5 with 150mg/kg of body weight of alloxan monohydrate. Group 2 rats were used as the experimental control. Fasting blood glucose of rats in all the groups were measured before and 72 hours after induction of diabetes. The rats were sacrificed after 72 hours and the pancreas was histopathologically analysed. The result showed a significantly high blood glucose level in group 2 rats indicating the diabetic state. The blood glucose level of rats in group 3 and 5 reduced significantly (p<0.05) when compared with the value of group 2 rats but not significantly different from group 1 value. Group 4 showed a significantly (p<0.05) high blood glucose level when compared with the base-line. The histopathology revealed atrophied islet of Langerhans in group 2 rats. Group 3 and 5, showed reviving islet cells and group 4 showed increased lymphoid follicles and neutrophills. The results suggest that the aqueous extract of V. amygdaliana has a protective effect against alloxan induced pancreatic damage and potential to revive damaged islet cells.
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Objective To explore the impacts of magnetic fields of different intensities on the superoxide dismutase (SOD) activity and malondialdchvde (MDA) levels in rat pancreatic islet cells under normal and hypoxic conditions.Methods Rat pancreatic islet cells were culured,and after 3 days were subjected to a magnetic field of either 44.8 mT,90.6 mT or 182.1 mT under either normal or hypoxic conditions.Control cells received no magnetic field exposure,SOD activity and MDA level were measured after 72 hr.Results The cultured cells grew linearly with optical density (OD) of 0.067 ± 0.021 after 2 days and 0.449 ± 0.113 afier 5 days.SOD activity was significantly lower in the three magnetic field intervention groups than in the control group.Under hypoxic culture conditions,in all the magnetic field intervention groups SOD activity increased at first and then deereased.Under normal culture conditions,MDA content was significantly higher in the 182.1 mT group than in the control group.In the other two groups it was significantly lower.Conclusion Magnetic field exposure can cause oxidative damage to pancreatic islet cells,at least rat cells in culture.Under hypoxic culture conditions a magnetic field can inhibit such damage.
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Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol-anchored cell surface antigen with an organ-dependent expression pattern in cancers; e.g., up-regulated in prostate cancer and down-regulated in gastric cancer. Previously it was reported that PSCA is not expressed in the normal pancreas but aberrantly expressed in pancreatic cancer. In this present study, we identified PSCA expression in islets of the pancreas by immunohistochemistry, which was co-localized with four islet-cell markers: insulin, glucagon, somatostatin and pancreatic polypeptide. In our investigation of the transcription start site of PSCA, we found a non-coding splicing variant of PSCA as well as authentic PSCA transcripts in mRNA samples from a normal pancreas. Both the transcripts were also identified in several pancreatic cancer cell lines. We previously reported that PSCA expression is correlated to the methylation status of the enhancer region in gastric and gallbladder cancer cell lines but not in pancreatic cancer cell lines, suggesting that PSCA expression is regulated in a diff erent mode in pancreatic cancer from that in gastric and gallbladder cancers.
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Antigens, Surface , Cell Line , Gallbladder Neoplasms , Glucagon , Immunohistochemistry , Insulin , Islets of Langerhans , Methylation , Pancreas , Pancreatic Neoplasms , Pancreatic Polypeptide , Prostate , Prostatic Neoplasms , RNA, Messenger , Somatostatin , Stem Cells , Stomach Neoplasms , Transcription Initiation SiteABSTRACT
Objective To study the effect of Coxsackie virus B3 (CVB3) infection on islet cells in vitro, and to explore the mechanism of islet cells caused by CVB3. Methods Bone marrow mesenchymal stem cells( BMSCs) were separated from the bone marrow and cultured. Then they were induced to differentiate into islet-like cells using nicotinamide and mercaptoethanol. Differentiated cells were detected by morphology , special staining and RT-PCR. Observe CVB3 infection on islet cells under inverse microscope and detect the specific gene fragment by RT-PCR. Results BMSCs showed half suspended shape and gathered to form a cluster after induction. Cells became red brown by dithizone specific staining. RT-PCR also proved the existence of mRNA expressing insulin. Infected islet cells appeared typical pathological changes like shrinks, refraction decreases. RT-PCR detected the desired specific gene fragment of 299 bp in infected islet cells. Conclusion CVB3 can directly injury islet cells, and damage the function of islet cells of secreting insulin.
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Objective To study whether eicosapentaenoate can decrease the apoptosis effects in-duced by palmitic acid in INS-1 or not. Methods Based on different condition, there were four groups in this study, including control group , EPA group, palmitic acid group, combination of EPA and palmitic acid group. The grow curve was detected by MTT, and the expressions of bax were detected by Western blot.Cell apoptosis was detected by caspase-3. ROS was detected by CM2H2DCFDA kit after 48h. Result The grow curve of combination of EPA and palmitic acid group was higher than that in plamitic group[24 h :(37.33±1.15)OD vs (30. 79 ± 1.55 )OD, P < 0. 01 ;48 h:(31.50 ± 1.56)OD vs (23.94 ± 1.10)OD, P<0. 01] . Caspase-3 activity and ROS and the expression of bax and SREBP1c in combination of palmitic acid and T0901317 group were lower than those in palmitic acid group[(3566. 67 ± 305.51 )OD vs (4233. 33 ±416. 33)OD]. Conclusion EPA can inhibit apoptosis in INS-1 induced by palmitic acid.
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BACKGROUND: Microencapsulation of islet cells has been studied for the treatment of type I diabetes to protect islets from immune attack by recipient cells during islet transplantation. In this study, we established optimal preparation conditions for islet microcapsules with good morphology and cell viability by employing an electrostatic droplet generator. METHODS: To obtain good quality islet microcapsules, various parameters such as the inner diameter of the electrostatic droplet generator nozzle, concentrations and infusion rates of alginate, electrostatic strength, and calcium chloride concentrations were tested. The size and shape of the capsules and cell viability were examined by light microscopy, and insulin secretion from the cells was determined by an ELISA analysis. RESULTS: The optimal preparation conditions for microencapsulation were a 0.35 mm inner nozzle diameter, a 1.75% alginate concentration, a 20 mL/hr alginate infusion rate, a 5 kV electrostatic potential, and a 75 mM calcium chloride. Under these conditions, over 90% of the capsules had a proper size (300~350 micrometer) and shape, and cell viability was 91%. Cell viability was maintained at greater than 80% even after the capsules were cultured for 2 weeks. However, glucose-induced insulin secretion of encapsulated islet cells was reduced by 85% compared to that of nonencapsulated cells. CONCLUSIONS: The results showed that an encapsulation technique using an electrostatic droplet generator is useful for making islet microcapsules with good morphology and cell viability. This technique is necessary to study microencapsulation using primary islets, enhancing glucose-induced insulin secretion, and to perform a functional evaluation of encapsulated islets in vivo in the near future.
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Alginates , Calcium Chloride , Capsules , Cell Survival , Drug Compounding , Enzyme-Linked Immunosorbent Assay , Glucuronic Acid , Hexuronic Acids , Insulin , Islets of Langerhans , Islets of Langerhans Transplantation , Light , MicroscopyABSTRACT
Objective To investigate the effects of differentiated 3T3-L1 adipoeytes on inflammation of rat islet cells,as well as the protective effect of a-lipoic acid on the inflammation in vitro.Methotis Rat islet cells were divided into three groups:the control group,the experimental co-culture system group(cocuhured with differentiated mature 3T3-LI adipoeytes)and the intervention group (cocuhured with mature 3T3-LI adipocytes containing 4 μg/ml a-lipoic acid).Insulin releasing lest wag performed for estinmting the function of islet cells in culture supernatant of difierent groups.At the same time,the expression level of IKKIβin islet cells Was detected by western blot and realtime PCR.Results There was significant decrease of insulin stimulation index (SI) in experimental co-culture system group compared with the control group and intervention group(1.0 ±0.1 vs 2.6±0.2,2.5±0.5 respectively;P<0.01),while,the mRNA(4.62±0.60 vs1.00±0.46 and 2.25±0.75;P<0.01)and protein expression of IKKβ were significandy increased in the experimental group as compared with the other two groups.Conclusions In the co-culture system of adipocytes/islet cells,impaired function of islet cells could be induced by IKKβ activation,IKKβ Was a key molecule in inflamnmtion signal pathway in islet cells and could be activated by 3T3-LI adipocytes.a-lipoic acid Was able to reverse the impaired function of islet cells by suppressing IKKβ expression.
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Objective To investigate the clinical features, diagnosis and treatment of malignant pancreatic endocrine tumor. Methods The clinical data of 38 patients with malignant pancreatic endocrine tumor who had been admitted to First Affiliated Hospital of Nanjing Medical University from January 1969 to December 2008 were analyzed retrospectively. Of all patients, 6 were with insulinoma, 23 with pancreatic polypeptide tumor, 4 with glucagonoma and 5 with pancreatic carcinoid. Results All patients except 1 with insulinoma were found with pancreatic lesion by imaging examination. The resection rate was 87% (33/38). Pathological examination found 7 patients with liver metastasis, 5 with lymph node metastasis, 1 with tumor thrombus in vessels and lymphatic vessels, and 28 with local invasion. Twenty-four patients were followed up, and neither recurrence nor metastasis was found except 1 patient with insulinoma who received reoperation for local recurrence and 1 patient with pancreatic carcinoid who received radiofrequency ablation for liver metastasis. Conclusions The diagnosis of pancreatic endocrine tumor mainly depends on imaging examination. The malignancy of pancreatic endocrine tumor is determined after the comprehensive analysis of preoperative imaging findings, intraoperative examination, post-operative pathological examination and the data obtained during follow-up. The malignant pancreatic endocrine tumor should be managed actively by resection because of its relatively low malignancy, high operative resectability and relatively good prognosis.
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abetes. The inhibition of the NF-κB expres-sion could be an effective strategy for protecting pancreatic islet cells.
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Objective To observe the effects of differentiation of mature islet cells of mice on marrowmesenchymal stem cells (mMSCs). To provide transplant source for islet cell transplantation in the treatment of diabetes. Methods The culture, isolation and passage of mMSCs was performed by using patch wall, cell shape was observed by confocal microscope, and flow cytometry analysis was used to determine their biological characteristics. The type Ⅳ collagenase was injected into common bile duct to digest the pancreas, and then gradient centrifugation was used to isolate islet cells. The transwell co-culture system was used for third generation of mMSCs and isolated islet cells, then inversion microscope was used to observe the cell growth and morphological changes, immunochemistry methods was applied to detect the expression of insulin in mMSCs, and insulin release test was performed to determine the secretion of insulin. The control group consisted of cultured mMSCs alone. Results The cells from mouse bone marrow were found to be in long spindle shape with large volume after 48 hours in culture. One week later the cells grew in the form of colony with serial subcultivation. The cell surface molecules including Sca-l, CD29, CD44, CD105 were positive with high level of expression;while the cell surface molecules including CD34, CD45 were negative, all of these results confirmed that the ceils were mMSCs. After 7 days of coculture with mice islet cells, part of mMSCs cells were positively stained by insulin immunohistochemisty, the insulin secretion was (16.83±0. 15)μIU/ml.Conclusions After cocultured with islet cells, mMSCs isolated from mouse bone marrow could differentiate into islet like cells. These cells may be used in the islet cells transplantation in the treatment of diabetes, which provided a solution to the problems of donor-shortage and immunologic rejection.
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In the present study, the effects of alpha lipoic acid (ALA) supplementation on glycemic control and lipid profile in streptozotocin (STZ)-induced diabetic rats have been evaluated. Sprague Dawley rats were divided into nondiabetic (NDM), diabetic without supplementation (No Suppl) and diabetic with ALA groups. ALA was orally administered once a day for 8 weeks with a dose of 100 mg/kg BW. Supplementation of ALA to STZ-induced rats prevented the severe damage to the islet cells of the pancreas and lowered the plasma glucose and glycated hemoglobin (HbA1c) levels. Supplementation of ALA also suppressed the increased of total cholesterol (TC), triglycerides and low density lipoprotein-cholesterol (LDL-C) levels in the plasma of diabetic rats as well as increased high density lipoproteincholesterol (HDL-C) levels. In conclusion, this study suggest that ALA may be effective in controlling glycemic status and improving dyslipidemia in streptozotocin-induced diabetic rats and has the potential in reducing cardiovascular complications due to diabetes mellitus.
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Rats , Streptozocin , Aminolevulinic Acid , Dyslipidemias , Thioctic AcidABSTRACT
Objective:To investigate the inhibition effects of different concentrations of ?-tocopherol on pancreatic islet cell viability,insulin secretion,anti-oxidation competence induced by streptozotocin. Methods:Pancreatic islet cells from Wistar rats aged 1 to 3 days were cultured in monolayer in vitro. and divided into 4 groups.Then,cell viability,insulin secretion,T-AOC,SOD activity,MDA level,NOS activity and NO2-/NO3- production were measured by differrent detection methods. Results:Streptozotocin significantly decreased cell viability,T-AOC activity,SOD activity and insulin release level(P0.05),that could not be blocked by ?-tocopherol. Conclusion:?-tocopherol can attenuate the damage of rats pancreatic islet cells induced by streptozotocin,the mechanisms of which may be that ?-tocopherol can reinforce the competence of scavenging free radicals of pancreatic islet cells and not related to NOS activity change.