Coompo Research Chemicals

The aging process leads to suppression of the antioxidative defence system and accumulation of lipid peroxidation products, while ginsenoside-Rd attenuates the oxidative damage, which may be responsible for the intervention of GSH/GSSG redox status.

Ginsenoside-Rd exhibited remarkable neuroprotection when presented during oxygen-glucose deprivation and reoxygenation, which may be ascribed to its antioxidative properties by reducing the intracellular reactive oxygen species and malondialdehyde production; increasing glutathione content; and enhancing the antioxidant enzymatic activities of catalase, superoxide dismutase and glutathione peroxidase. Additionally, Ginsenoside-Rd could stabilize the mitochondrial membrane potential and attenuate apoptotic death of hippocampal neurons after oxygen-glucose deprivation exposure. These findings suggested that Ginsenoside-Rd may be a potential neuroprotective agent for cerebral ischemic injury and should encourage further in vivo studies on stroke to explore the potential neuroprotective efficacy of Ginsenoside-Rd. Ginsenoside-Rd, as an inhibitor, remarkably inhibits Ca2+ entry through receptor- operated and store-operated without effects on voltage-dependent inward Ca2+ current and Ca2+ release in vascular smooth muscle cells.

The effect of ginsenoside-Rd in ischemic-reperfused rats was examined. In control rats, blood and renal parameters and the activities of antioxidative enzymes in renal tissue deviated from the normal range, indicating dysfunction of the kidneys. In contrast, when ginsenoside-Rd was given orally for 30 consecutive days prior to ischemia and reperfusion, the activities of the antioxidation enzymes superoxide dismutase, catalase and glutathione peroxidase were higher, while malondialdehyde levels in serum and renal tissue were lower in the treated rats than in the controls. Decreased levels of urea nitrogen and creatinine in serum demonstrated a protective action against the renal dysfunction caused by ischemia and recirculation. On the other hand, it was demonstrated that ginsenoside-Rd affected cultured proximal tubule cells subjected to hypoxia-reoxygenation, probably by preventing oxygen free radicals from attacking the cell membranes.

Ginsenoside Rd significantly inhibits HeLa cell proliferation, and induces cell apoptosis through down-regulating Bcl-2 expression, up-regulating Bax expression, lowering the mitochondrial transmembrane potential, and activating the caspase-3 pathway. Thus, Ginsenoside Rd could serve as a lead to develop novel chemotherapeutic or chemopreventive agents against human cervical cancer.