Ginsenoside Rd COX inhibitor

Ginsenoside Rd is a selective and competitive Ca2+ receptor antagonist and herefore, can suppress calcium influx after cytotoxic injuries. This compound administration dose-dependently suppresses glutamate-induced DNA laddering and apoptosis through the suppression of glutamate-induced caspase-3 activation and Ca2+ entry. Exposure to this chemical can also protect mitochondria against calcium-induced damages through downregulation of reactive oxygen species generation, suppression of mitochondrial membrane potential hyperpolarization, and amelioration of mitochondrial swelling[1]. It is a potent in vitro inhibitor on the chymotrypsin-like activity of 26S proteasome[2].

Ginsenoside Rd treatment prior to and/or following an ischemic stroke can reduce infarct volume, increase neuronal survival, and enhance cognitive and neurological functions. Administration of this compound to a Sprague-Dawley rat has been shown to downregulate ischemic stroke-induced tau protein phosphorylation at Ser199/202 and PHF-1 sites through the downregulation of glycogen synthase kinase-3β and to enhance ischemia-induced cognitive impairment. This compound administration has also been shown to upregulate the protein kinase B/AKT pathway and, from this, suppress glycogen synthase kinase-3β activity. Its administration after tMCAO upregulates glial glutamate transporter-1 (GLT-1) expression and promotes glutamate clearance in rats. Pretreatment with this chemical (10 mg/kg) inhibits poly(ADP-ribose) polymerase-1 and consequently downregulates apoptosis-inducing factor translocation and nuclear factor-kappa B p65 subunit nuclear accumulation in Dawley rats suffering from right middle cerebral artery occlusion[1].