Diabetic nephropathy is a complication of diabete and its incidence is increasing obviously these years. The pathogenic mechanisms of DN are complex, with multiple factors involved such as the glycometabolism disorders , hemodynamic changes, aldose reductase pathway activation, alterations in cytokines, oxidative stress, protein kinase C activation, lipid metabolism disorders and genetic susceptibility etc, which are not completely clear yet. Thus, the research progress of DN pathogenesis is to be reviewed.

AIM: To investigate the relationship betw een ADRP and the development of atherosclerosis. METHODS: Antisense oligodeoxynucleotide of mouse ADRP was constr ucted. The mouse peritoneum macrophages were cultured with Ox-LDL or Ox-LDL plus the antisense fragment. The cellular cholesterol was measured and the expressio n of ADRP was observed with RT-PCR and western blotting. New Zealand white rabbi ts were fed with high cholesterol chow for 12 weeks. The levels of serum lipid a nd cholesterol content of aortic wall were investigated. The areas of fatty stre ak of the aortas was measured after staining with Sudan Ⅳ. The aortic, and live r specimens with HE and immunohistochemistry staining were observed under light microscopes. RESULTS: Antisense oligodeoxynucleotides of mouse ADRP decreased cellular cholesterol ester, induced cellular lipid droplets and the expression of ADRP. The expression of ADRP was induced by high-cholesterol-diet feeding in rabbit atherosclerotic lesions. The fatty streak of the aorta with immunohistoch emistry staining was strongly positive for ADRP in animals fed with high cholest erol chow, and the liver was negative with or without high cholesterol chow. CONCLUSIONS: The expression of ADRP in vessel walls is related t o the atherosclerosis, and has a potential role in lipid accumulation in macroph ages and pathogenesis of atherosclerosis.

AIM: Based on the finding of adipophilin expression with the increase in cellular cholesterol, the aim of the present study was to look for the active site of adipophilin in cellular cholesteryl metabolism. METHODS: Mouse peritoneal macrophages were incubated with 80 mg/L Ox-LDL (Ox-LDL group) or 80 mg/L Ox-LDL plus 1 mmol/L adipophilin antisense oligonucleotides (Ox-LDL+antisense group), respectively. At the various time points, the incubated cell samples were observed with adipophilin immunofluorescence staining, flow cytometric analysis and cellular cholesterol analysis. RESULTS: The Ox-LDL+antisense group cells contained significantly lower cholesteryl ester (19.9?1.9) mg/g (protein) than that of cells in Ox-LDL group (46.6?3.4) mg/g (protein) at 4 days. From 12 h, expression of adipophilin in Ox-LDL group increased more quickly than that of the cells in Ox-LDL+antisense group. At day 4, the level of adipophilin expression in Ox-LDL group was significantly higher than that in Ox-LDL+antisense group. During the observation, the amount of Ox-r[CL-3H] LDL taking up increased gradually in both groups, however, from day 1 the taking up amount in Ox-LDL+antisense group was less than that in Ox-LDL group. There was a statistical difference between the two groups from day 2 to day 4. From 6 h to day 2, the relative ACAT activity increased in both groups. The relative ACAT activity kept unchanged from day 2 to day 4 in the two groups. At day 2, the relative ACAT activity in Ox-LDL+antisense group was significantly lower than that in Ox-LDL group. Correlative analysis between activity of ACAT and adipophilin expression showed than R2 were 0.6176 and 0.8212 (P