Objective To establish a model of renal ischemic/reperfusion in rats and to observe whether propofol protects kidney from this injury, and to deduce a possible mechanism.Methods Ninty-nine male SD rats with right nephrectomy were randomly divided into three groups according to the different treatments to left kidney: Control group (n=26), IR group (n=35), IR+Pro group (n=38). The left kidney was exsected and blood samples were collected 0, 3, 12, 24, 72 h postsurgery respectively. Renal morphology dyed with HE was observed with light microscopy . Immunohistochemistry was used to detect the expression of apoptosis proteins including BCL-2、BAX、caspase 3、cytochrome C.Results Renal ischemia-reperfusion induced tissues injury, the severity of injury sequence was as follows: proximal convoluted tubule, distal convoluted tubule, collecting duct, renal corpuscle; According to the results of IHC, the expression of BAX, caspase 3, and cytochrome C in IR group were more than that in control group, and BCL-2 level was stable. The protective protein (BCL-2) level was higher and the proteins (BAX, caspase 3, and cytochrome C) inducing apoptosis were lower in IR+P group than that of IR group (P

AIM: To explore the effect of aspirin on inducible nitric oxide synthesis and gene expression under inflammation in endothelial cells. METHODS: Using NADPH, Griess methods and RT-PCR, the activity of isozymes of NO synthase (NOS), nitric oxide (NO) level, and iNOS mRNA expression were examined respectively. Also, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content and cell viability were measured. RESULTS: Aspirin (3 mmol/L) reduced inducible NO production and NOS activity(P

AIM: To explore the regulatory effects of ferritin expression and intracellular iron change on aspirin resistance to oxidative damage in endothelial cells. METHODS: Using ELISA to measure the levels of ferritin expression under different aspirin concentrations, in the presence of iron cheltor desferioxamine and add to FeCl 3. Then using RNA-protein bandshift assay and RT-PCR to examine the activation of IRP and the expression of IRP 2 mRNA onaspirin induced ferritin formation. RESULTS: Aspirin at low concentration (0.1mmol/L) induced significant increase in ferritin expression in a concentration-dependent fashion up to 25% over basal levels. Aspirin induced cytoprotection from H 2O 2 damage increased significantly following ferritin formation in endothelial cells.However, in the presence of iron chelator desferrioxamine, aspirin enhanced ferritin synthesis was abrogated with a 3 fold increase in the activity of IRP and significant increase in IRP 2 mRNA level. In contrast, FeCl 3 and aspirin both increased the level of induced ferritin synthesis with significant decrease in IRP activity and IRP 2 mRNA level. CONCLUSION: The effect of aspirin induced ferritin synthesis on resistance to oxidative damage in endothelium was operated through down-regulating IRP activation and IRP 2 mRNA level.