Ginsenosides Protect Apical Transporters of Cultured Proximal Tubule Cells from Dysfunctions Induced by H2O2

Oxidative stress has been implicated as a primary cause of renal failure in certain renal diseases. Indeed, renal proximal tubule is a very sensitive site to oxidative stress and retains functionally fully characterized transporters. It has been reported that ginsenosides have a beneficial effect on diverse diseases including oxidative stress. However, the protective effect of ginsenosides on oxidative stress has not been elucidated in renal proximal tubule cells. Thus, we examined the effect of ginsenosides on oxidative stress-induced alteration of apical transporters and its related mechanism in renal proximal tubule cells. In the present study, hydrogen peroxide (H2O2) (>10–5M) inhibited α-methyl-D-glucopyranoside uptake in a dose-dependent manner (p < 0.05). It also inhibited Pi and Na+ uptake. At a concentration of 20 µg/ml, total ginsenosides significantly reduced H2O2-induced inhibition of apical transporters. In contrast, protopanaxadiol (PD) and protopanaxatriol (PT) saponins exhibited a less preventive effect than total ginsenosides (p < 0.05). Furthermore, we examined its action mechanism. H2O2 increased lipid peroxide formation, arachidonic acid (AA) release, and Ca2+ uptake. These effects on H2O2 were significantly prevented by total ginsenosides and PD or PT sanponins. However, total ginsenosides appear to be more protective than PD and PT saponins (p < 0.05). In conclusion, ginsenosides prevented H2O2-induced inhibition of apical transporters via a decrease in oxidative stress, AA release, and Ca2+ uptake in primary cultured renal proximal tubule cells.