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- W2370785518 abstract "Objective To study whether glutamic acid decarboxylase(GAD) purified from pig brain can prevent type Ⅰ diabetes in non obese diabetic(NOD) mice and influence the expression of GAD65 in islets. Methods GAD 50 μg mixed with Freund incomplete adjuvents(FIA) 50 μl was injected intreperitoneally(ip) into 32 NOD female mice at 4 weeks old, FIA was injected alone to 19 mice as control. All mice had blood glucose and body weight measured weekly. One single injection of cyclophosphamide(CY) was given to accelerate the diabetes at 8 weeks old. After death of the mice at 20 weeks old, the levels of C peptide and autoantibodies to GAD were detected and the pancreatic histopathology was observed too. The expression of GAD65 mRNA was measured using reverse transcriptase(RT) PCR technique. Results (1)GAD reduced the total incidence of type Ⅰ diabetes to 6 25% as compared with the FIA group(73.68%,P0.01) and delayed its onset time(4 weeks vs 1.5 weeks after CY acceleration).(2)The insulitis score and the severity of insulitis in GAD mice were lower than that of the FIA group(P0.05).(3) The C peptide levels were higher significantly in GAD group as compared with the FIA group(P0.05),but the prevalence of GAD antibody was no significantly different between the two groups.(4)The levels of expressing products in islets of GAD mice (1.616±0.146) were much higher than those of FIA mice(1.226±0.018,P0.05). Conclusion GAD protected the NOD female mice from getting diabetes and insulitis. Its mechanism may be related to induction of immune tolerance by increasing the GAD65 expression in islets." @default.
- W2370785518 created "2016-06-24" @default.
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- W2370785518 date "2000-01-01" @default.
- W2370785518 modified "2023-09-25" @default.
- W2370785518 title "Glutamic acid decarboxylase may protect type I diabetes in non obese diabetic mice through inducing immune tolerance" @default.
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