| Diabetes is an important modern disease. Type 1 diabetes was considered as an autoimmune disease before induced by inheritance and environment factors, in pathogenesis, cell-mediated immunity was main reason, and inflammatory factor can induce apoptosis via oxygen-derived free radical. Likewise, the pathogenesis of type 2 diabetes was believed to be insulin resistance, βcell of islet degeneration and exhaustion caused by inheritance and environment factors. The latest epidemiology research shows that type 2 diabetes was also an inflammatory disease, and the generating of disease had relation with C reaction protein, TNF, ILs, plasminogen activator inhibitor, adiponectin, and leptin. As far as type 2 diabetes is concerned, inflammatory reaction is reason not only for insulin resistance, but also for apoptosis; reasons leading to chronic diabetes complication, which also derives from inflammation, are still reasons for diabetes episode. The possible pathogenesis in common for type 1 and 2 diabetes is that oxygen-derived free radical, which origins from inflammatory factors catalyzed by NOS (nitricoxide synthase) and cox, results in diabetes through inducing dysfunction and apoptosis of pancreatic islet cells. Other study also proved that there existed regeneration of pancreatic βcells in type 1,2 diabetes in the whole life, furthermore, regeneration and reconstruction capacity of islet cells, the functions of stimulating factor and inhibiting factors may be play a more important role in pathogenesis. Because the number of patient suffering diabetes is continually increasing, diabetes has become a focus in the research of modern medicine and biology. The etiology study of diabetes is especially concerned. In this study, rat diabetes model was produced with the method of low-dose of STZ (MLDS). With the application of histopatholoty, immunohistochemistry, laser confocal scanning, and Western blotting analysis , apoptosis, regeneration, oxygen-derived free radical and TGF-βwhich relate to βcell of islet of DM rat were observed and analyzed, the occurrence and development mechanism of diabetes is discussed, in order to provide theory basis for the prevention and therapy of diabetes. In experiment are carried out in the following three steps: 1. Establish diabetes model with Wistar rat and analyze oxygen-derived free radical, apoptosis and regeneration related factors. 2. The effect of insulin on related factors such as oxygen-derived free radical, apoptosis and regeneration on DM rat's pancreatic islet. 3. Observ DM rat for three months and re-analyze the related factors such as oxygen-derived free radical, apoptosis and regeneration in the group with blood sugar<7.8, the group with blood sugar>1.2 and insulin treatment group. In the experiment, inflammatory cell infiltration was observed with HE staining; oxygen-derived free radical with NO synthase and immunohistochemistry staining; apoptosis with Caspase-8 immunohistochemistry staing; cell proliferation with PCNA immunohistochemistry; label amount of βcell with aldehyde-fuchsin, TGF-βwas analyzed with immunohistochemistry staining and Western blotting; the expressions and relation in location of insulin, PCNA and TGF-βwere also confirmed with laser focus. Result: 1. Wistar rat can be induced into diabetes model successfully by the method of low-dose STZ (MLDS); after injecting of 30mg/kg /time and four times in total, the model forming rate is nearly 90%; there is significant difference (P<0.05) in blood sugar level between model group and normal controlled group, which means that blood sugar in model group is clearly higher than in controlled group; on the contrary, the difference in insulin level is also significant (P<0.05) between model group and controlled group, but higher in the latter. The pathologic change of pancreas of DM rat is that amount ofβcell of islet reduces, and inflammatory cells infiltration mainly includes lymphocytes and monocytes. Vacuolation of pancreatic βcell makes lack of...
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