Ginsenoside Rg5

Ginsenoside Rg5 is a ginsenoside originally isolated from P. ginseng that has diverse biological activities, including anticancer, anti-inflammatory, neuroprotective, and antioxidant properties. It inhibits the growth of HeLa and MS751 cervical cancer cells (IC50s = ~2.5-10 μM) and induces apoptosis in a concentration-dependent manner. Ginsenoside Rg5 (5 and 10 μM) inhibits LPS-induced increases in IL-1β, TNF-α, COX-2, and inducible nitric oxide synthase (iNOS) protein levels in murine alveolar macrophages. It also inhibits LPS-induced increases in the number of neutrophils and protein levels of IL-1β, TNF-α, COX-2, and iNOS in lung in a mouse model of acute lung inflammation when administered at a dose of 10 mg/kg. In a rat model of Alzheimer's disease induced by streptozotocin (STZ;), ginsenoside Rg5 blocks STZ-induced increases in amyloid-β accumulation in the hippocampus and cerebral cortex and prevents STZ-induced decreases in step through latency time in a passive avoidance foot-shock test in a dose-dependent manner.

Ginsenoside Rg5 is an aromatase inhibitor from Panax ginseng leaves. Also, it ameliorates cisplatin-induced nephrotoxicity in mice through inhibition of inflammation, oxidative stress, and apoptosis.

Ginsenoside Rg5 is a diol-containing ginsenoside, that occurs naturally in Panax ginseng. It is found to be a promising agent in the treatment of Alzheimer′s disease.

Ginsenoside Rg5 is a major constituent of steamed ginseng; shows anti-inflammatory effect. IC50 value:Target:in vitro: Rg5 inhibited the expression of proinflammatory cytokines, IL-1β and TNF-α, as well as inflammatory enzymes, COX-2 and iNOS in LPS-stimulated alveolar macrophages. Rg5 also reduced LPS-induced phosphorylation of IL-1 receptor-associated kinases (IRAK)-1 and IKK-β, as well as the degradation of IRAK-1 and IRAK-4. Rg5 inhibited the phosphorylation of NF-κB as well as the translocation of p65 into the nucleus. Angiogenic activity of Rg5 was highly associated with a specific increase in insulin-like growth factor-1 receptor (IGF-1R) phosphorylation and subsequent activation of multiple angiogenic signals, including ERK, FAK, Akt/eNOS/NO, and Gi-mediated phospholipase C/Ca(2+)/eNOS dimerization pathways. The vasodilative activity of Rg5 was mediated by the eNOS/NO/cGMP axis. IGF-1R knockdown suppressed Rg5-induced angiogenesis and vasorelaxation by inhibiting key angiogenic signaling and NO/cGMP pathways. Ginsenoisde Rg5 or Rh3 (10 mg/kg) significantly shortened the escape latencies prolonged by treatment with scopolamine on the last day of training trial sessions in Morris water maze task. Furthermore, ginsenosides Rg5 and Rh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC50 values of 18.4 and 10.2 μM, respectively. in vivo: Rg5 improved cognitive dysfunction and attenuated neuroinflammatory responses in streptozotocin (STZ)-induced memory impaired rats. Cognitive deficits were ameliorated with Rg5 (5, 10 and 20mg/kg) treatment in a dose-dependent manner together with decreased levels of inflammatory cytokines TNF-α and IL-1β (P<0.05) in brains of STZ rats.