| Objective: The mechanism of 2 type diabetes and 1 type diabetes is different, the former can induce the disorder of glycometabolism and lipid metabolism. It is well known that high blood sugar can induce cataract, but the relationship between the lipid metabolism and the cataract is hardly implored by now, our study want to implore the relationship between the lipid metabolism and the cataract which supervened with 2 type diabetes, in addition, our also detect the relationship between the apoptosis of LECs(lens epithelial cells) and the cataract which supervened with 2 type diabetes, lastly our study implored the therapeutical effect of the rosiglitazone to the cataract which supervened with 2 type diabetes.Methods: Divide the rats into three groups: A ,B and C . A group contains twenty rats(normal control group), B group contains twenty rats(high fat group), C group contains forty rats(diabetes model group). Feed the rats in A group ordinary forage, and feed the rats in B and C groups high fat and high sugar forage. After feeding four weeks inject the rats in C group little dosage STZ to make diabetes model. After two weeks of injection, measure the blood sugar, regard the rat whose sugar tolerance anomaly as diabetic model rat. Then divide the diabetic model rats into three groups: C1 group(kill after feeding twelve weeks), C2 group(from the twelfth week treat the rats high pressure antiseptic solution by intragastric administration, kill them on the twentieth week ), C3 group(from the twelfth week treat the rats the rosiglitazone dissolved by high pressure antiseptic solution (1.42mg·kg-1·d-1) by the way of intragastric administration, then kill them on the twentieth week ). After the rats become diabetic model, measure their blood sugar every week, observe the opacity of the lens, and record the level of the opacity. Before killing the rats, cut their tails and measure the blood-fasting sugar. After anaesthetizing the rats, take blood from their abdomen cardinal vein. Measure the insulin level of blood plasma by the method of radio-immunity, and measure the level of blood fat by biochemical analyzer. Take out the eyeball, tear its anterior capsular, then spread the anterior capsular on the glass slide, later fix it by the alcohol glacial acetic acid fixative solution EAA(three share of dehydrated alcohol adds one share of acetic acid ), detect the apoptosis of the lens epithelial cells with the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL), that is under the light microscope count three no marginal visual fields in every stretched preparation, and count two hundred cells in every stretched preparation, then calculate the percentage of the apoptotic cell; analyze the correlation of the level of the crystal opacity with the percentage of the apoptosis of the LECs.Results: 1. General condition: 26 out of the 40 rats became the diabetes model rats, the rate is 65 percent, the blood-fasting sugar,plasma insulin and triglyceride of the diabetes model rats all significantly increased compare with that of the control group rats(p<0.05), their cholesterol has no apparent changes on the 12th week, but increased significantly on the 24th week(p<0.05). Compared with the 12th week diabetes rats the 24th week diabetes rat's blood-fasting sugar and plasma insulin have no apparent change, while their triglyceride and cholesterol increased significantly(p<0.05). Except the blood sugar being normal in the high fat group, other indexes have no significant difference with the diabetes group simultaneously. The blood plasma insulin of the rosiglitazone intervention group decreased to the normal level, their blood sugar,triglyceride and cholesterol decreased significantly than the non-intervention group (p<0.05), while the three indexes were also significantly high than the control group(p<0.05). 2. The condition of lens: Throughout the experimentation all the lens kept crystal in both the control group and the high fat group rats. From the seventh week there beg...
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