| Objective: Glucagon like peptide1(Glucagon-like peptide1, glp-1)analogues-the Liraglutide in obstructive sleep apnea hypopnea syndrom(Ostructive sleep apnoea/hyopnoea syndrome, OSAHS) in the rat model of theinfluence and mechanism of islet beta cells. Methods: Experiment randomlydivided: often oxygen in the control group (UC)12, intermittent hypoxia group(IH)24, oxygen control group rats often given oxygen, conventional breeding.Intermittent hypoxia group of intermittent hypoxia in rats (nitrogen and oxygencycle) mode. Building after8weeks, two groups of rats were extract primary rat islet beta cells, UC group were randomly divided into control group and highsugar stimulation (25.6mmol/L)6ones, IH group were randomly divided intoOSAHS group and lalu peptide (10,50,100nmol/L) intervention group fourgroups (6only, the rest of the group was given equal balanced salt solution. WithDTZ staining method to identify islet beta cells. By ELISA method for the abovethree groups of rat islet beta cells in the supernatant of tumor necrosis factoralpha and interleukin8,8-different prostaglandins, glutathione peroxidase(gsh-px). Using flow cytometry instrument detection rat islet beta cell apoptosis.Using Western Blot method to detect islet beta cells apoptosis related proteinsCaspase3expression level, immunohistochemical staining method to detect isletbeta cells apoptosis related proteins Caspase3expression level.Results: IHgroup and high sugar stimulation, respectively, compared with UC group, ratislet beta cells in supernatant of tumor necrosis factor alpha and interleukin8,8-different prostaglandins expression levels rise, GSH Px express, islet beta cellsapoptosis rate increases, apoptosis related proteins Caspase3expressed in isletbeta cells increases, the difference was statistically significant (P <0.05).Compared with OSAHS group, the lalu peptide intervention group aftertreatment on the islet beta cells supernatant of tumor necrosis factor alpha andinterleukin8,8-different prostaglandins expression level decreased, GSH Pxexpress, islet beta cells apoptosis rate low, apoptosis related proteins Caspase3expressed in islet beta cells, the difference was statistically significant (P <0.05),and high concentration group is relatively low and medium concentration effectis more significant.Conclusions: Oxidative stress is involved in thepathophysiology of OSAHS animal models, and this process has damage on theislet beta cells, intermittent hypoxia caused by oxidative stress may be important mechanism of OSAHS prompted islet beta cell damage, high sugar stimulatepancreatic islet cells produce oxidative stress and islet cell apoptosis, glucagonlike peptide1analogues-the lalu peptide may adjust the oxidation of activematerial content within the islet beta cells, thus reduce islet beta cells in theoxidative stress injury, The islet beta cells have a protective effect. |
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