Objective To assess the protective effect of remifentanil on cultured human hepatocytes against anoxia-reoxygenation injury. Methods Cultured hepatocytes were divided into 5 groups: group C receiving normoxia as control; groups AR, R, CH, R+CH receiving 15-hour xypoxia followed by 5-hour reoxygenation (group R receiving 5 ng/ml remifentanil, group CH 10 ?mol/L chelerythrine, group R+CH 5 ng/ml remifentanil and 10 ?mol/L chelerythrine before reoxygenation). The content of MDA in the hepatocyte mitochondria were measured. The rate of apoptotic cells was measured by flow cytometry. The expression of protein kinase C mRNA was measured by RT-PCR. Results Anoxia-reoxygenation caused dramatic increase in the content of MDA, the rate of apoptotic cells and the expression of protein kinase C mRNA. The three indexes mentioned above of groups R and CH were between that of groups C and AR (P

To investigate the effects of oleanolic acid (OA) on the proliferation, migration and the formation of tube-like structure in human vascular endothelial cells (HUVECs). MTT assay, flat plate scarification, Transwell plates and matrigel-induced tube formation assay were performed to detect the effects of OA on proliferation, migration and tube formation. MTT assay showed that the inhibition rates of HUVECs treated with 60 and 100 microg x mL(-1) of OA for 24 h were 19% and 83% respectively. Treatment of HUVECs significantly inhibited the cell migration in a dose-dependent manner. The vascular indexes of HUVECs treated with 40 and 60 microg x mL(-1) OA were 33% and 20% respectively. Western blotting analysis showed that treatment of the cells with OA significantly attenuated the expression and secretion of VEGF. Additionally, VEGF could in part reverse the effects of OA on migration and tube formation of HUVECs. In conclusion, OA inhibits the proliferation, and VEGF plays an important role in OA induced decreased migration and tube formation of HUVECs.

Objective To compare the diuretic efficacy of torasemide as a 2-hour continuous infusion and as a bolus injection of equal dose in patients with nephrotic syndrome,and to investigate a preferable administration mode of torasemide for these patients.Methods Twenty-three hospitalized patients were randomized to receive torasemide 20 mg or 40 mg per day by either 2-hour intravenous infusion or bolus injection,and interchanged after 48 hours of washout.Results Patients received torasemide by 2-hour intravenous infusion exhibited significantly higher daily urinary volume,chloride excretion,sodium excretion and fractional excretion of sodium (FENa) within 24 hours than those by bolus injection (P ＜ 0.05).Significantly lower bound-state torasemide excretion,higher ratio of urinary volume to torasemide excretion and a markedly larger area under the curve in the plasma concentrationtime profiles were also observed in the infusion group (P ＜ 0.05).Conclusion 2-hour continuous infusion delivers a better diuretic effect compared with a bolus injection of equal dose of torasemide in patients with nephrotic syndrome.

Objective: To explore the role of ROCK1 in oxidized low-density lipoprotein (ox-LDL) induced podocyte injury and its possible mechanism. Methods: The conditionally immortalized mouse podocyte cells were cultured in vitro and exposed to 20 μg/ml ox-LDL for 24 h. Western blotting was used to analyze the expression level of p-MYPT, nephrin, LC3-Ⅱ, p62, p-ULK1 in groups of control, ox-LDL, ROCK1 siRNA with ox-LDL, wtROCK1 with ox-LDL. Podocytes were incubated with DiI labeled ox-LDL for 4 h and fluorescence microscope was used to analyze lipid distribution. Results: Compared with control group, ox-LDL increased cell cholesterol accumulation, activated ROCK along with decreased nephrin, LC3-Ⅱ(P<0.05), and increased p62, and p-ULK1 expression (P<0.05). Over-expression of ROCK1 significantly decreased the expression of nephrin and LC3-Ⅱ, but up-regulated the levels of p62, p-ULK1 and cell cholesterol accumulation in ox-LDL stimulated podocytes (P<0.05). In contrast, Inhibition of ROCK1 protected podocyte by improved lipophagy. Conclusion ROCK1 mediated disfunction of lipophagy contributes to the ox-LDL induced podocyte injury.