[Proteomics analysis of erythrocyte membrane in rats with high altitude polycythemia before and after intervention with salidroside].

To investigate the effect of salidroside on the proteomics of erythrocyte membrane in high altitude erythrocytosis(HAPC) rats, in order to explore the mechanism of salidroside in improving HAPC based on the proteomics analysis. First, HPAC rat models were established, and 16 rats were randomly divided into HAPC model group and salidroside(100 mg·kg~(-1)) treatment group(8 rats per group). Saline was administered to the HAPC model group, while salidroside treatment group was given 100 mg·kg~(-1) salidroside once a day. After continuous oral administration with salidroside for 40 days(once a day), blood was collected from the femoral artery to obtain total red blood cell membrane proteins. Two-dimensional electrophoresis was used to separate total proteins. The two-dimensional electrophoresis of erythrocyte membrane proteins was analyzed before and after salidroside intervention, and the proteins with significant differences were identified by mass spectrometry. Finally, biological functions were analyzed using bioinformatics. A two-dimensional electrophoresis method was used to establish a protein expression profile with a high resolution and reproducibility of erythrocyte membranes in HAPC rats. Salidroside treatment significantly changed 18 protein spots in the 2-DE map of erythrocyte membranes, of which 13 proteins were up-regulated and 5 proteins were down-regulated. Eight differential proteins were successfully identified by mass spectrometry. Moreover, bioinformatics analysis found that these differential proteins were involved in such biological processes as oxidative stress, redox, and peroxisome pathway, which are mainly associated with peroxisome and MAPK signaling pathways. Therefore, salidroside could significantly change the expressions of erythrocyte membrane proteins in HAPC rats. Eight differential proteins were identified by a proteomic-based approach. The differential proteins were involved in such biological processes as oxidative stress, redox, peroxisome pathway.

Na+/H+ exchanger inhibitor prevented endothelial dysfunction induced by high glucose.

The aims of this study were to examine whether cariporide, a selective Na+/H+ exchanger inhibitor, has protective effects against endothelial dysfunction induced by high glucose in vitro and to investigate the potential mechanisms. Exposure of rat aorta rings to high glucose (44 mmol/L) for 6 hours caused an inhibition of acetylcholine-induced endothelium-dependent relaxation but had no effect on sodium nitroprusside-induced endothelium-independent relaxation. Treatment with cariporide (0.01, 0.1, 1 micromol/L) of aortic rings incubated with high-glucose medium attenuated the impaired endothelium-dependent relaxation in a dose-dependent manner. Furthermore, high glucose resulted in an increase of malondialdehyde and a decrease of superoxide dismutase activity in rat aorta rings, and these effects were reversed by cariporide. In addition, cariporide was able to inhibit the activation of Na+/H+ exchanger induced by high glucose in cultured endothelial cells. These findings suggest that the endothelial dysfunction induced by high glucose in vitro is caused by the activation of Na+/H+ exchanger.