| Lipid metabolism abnormality have close relationship with renal disease, it is not only one of the clinical symptoms of the renal disease, but also has participated the occurrence and development of the renal disease. Since 80's, more and more researchers have paid attention to the relations between albuminuria, glomerulosclerosist and the abnormality of lipid metabolism. Now, we have not make clear of the mechanism of gene regulation in lipid metabolism. In recent years, many animal experiments and experiments in laboratory discover that one kind of cellular membrance glycoprotein called SR (scavenger receptor) take a very important role in the atherosclerosis and lipid metabolism. Renal glomerulus is a exceptive capillary mass, its mesangial cell is similar with vascular smooth muscle in anatomy, origin, histochemistry, and constriction function, etc. we all know that glomerulosclerosis and atherosclerosis are alikeness very much, so we can conceive that they have the same mechanism. Another research finds that there also are scavenger receptor in the glomerulus mesangial cells. From all of this, we can consider that there is a really relationship between the gene expression of scavenger receptor and disturbed lipid metabolism. At present, many researchs of the scavenger receptor have emphasized the cardio-vascular field, i.e. the effects of gene expression of scavenger receptor in atherosclerosis. In renal disease, Domestic and international , we can only see the report that phorbol12-myristate13-acetate and angiotensin â…¡ induce the gene expression of scavenger receptor on mesangial cell in vivo and the influence of ACEI. There are no report about the effects of fluvastatin on gene expression of scavenger receptor in experiment animals. Adriamycin nephrosis in rats is a really typical animal model in nephritic syndrome reseaching nowadays. It is similar with the human minimal change nephropathy, heavy abluminuria, low ablumiemia, high lipitoemia are the mainly clinical characters. the pathogenesis relates to the production of adriamycin induce [O] and peroxide-lipid. this experiment do some work on the adriamycin nephrosis in rats, measure the quantity of protein in urine, the level of MDA, SOD in nephritic tissue, the levels of serous protein, lipid and gene expression of scavenger receptor. we also observe the effects by adding HMG-COA-fluvastatin and the changes of pathology under electron microscope .the objective is discover the effects of the disturbed lipid metabolism in the process of renal disease occurrence and development from molecular levels. it can offer the theory basis of clinicial treatment. Choose 30 male wiatar rats, weigh 210-250g, divide into 3 groups in random, etc, the normal group has 6 rats. adriamycin nephrosis group has 11 rats, the treatment adriamycin nephrosis with fluvastatin has 13 rats. injecting adriamycin in veins of the rat's tail only once, we can get the rats with adriamycin nephrosis. 0.9%NaCl dissolve the adriamycin, we can get 0.26% adriamycin solution. we inject this solution in the vein of tail comply with 0.25ml/100g measured. after 7 days, choose 13 rats randomly as fluvastatin- treatment group, complying with 10mg/kg measured each day, injecting fluvastatin straightly in the stomaches, the other groups we use only water correspondencely. after injecting the adriamycin 3 days, 7 days, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, and 7 weeks, we collect the all urine in 24 hours, then measure the volume and the levels of protein using biuret method. in detail, get 1 ml urine and 1ml solution as contract, each add into 4ml biuret, heat preservation, and measure the absorbency at A540. from the standard curve, we can the get the levels of protein in urine. at 7 weeks, kill the rats, we can get the serum, using L-20 biochemistry auto-analysis apparatus, we get serum total protein (TP), albumin (ALB), total cholesterol (TC), total triglyceride (TG), high dense lipoprotein (HDL). Low dense lipoprotein (LDL), apolipoprotein A (Apo...
|
PDF Full Text Request