Ginseng ingredients

Ginsenoside F2 has the anti-cancer activity, it induces apoptosis in breast cancer stem cells (CSCs) by activating the intrinsic apoptotic pathway and mitochondrial dysfunction, also induces the formation of acidic vesicular organelles, recruitment of GFP-LC3-II to autophagosomes, and elevation of Atg-7 levels, suggests that F2 initiates an autophagic progression in breast CSCs.

Ginsenoside Rk1, one of the main elements of Sung Ginseng, has been confirmed as a new endothelial barrier enhancer recently and has anti-cancer activity, the mechanism involves coordination between inhibition of telomerase activity and induction of apoptosis.

20(R)-Ginsenoside Rg3 has shown multiple pharmacological activities and been considered as one of the most promising approaches for fatigue treatment, however, 20(R)-Ginsenoside Rg3 has a low bioavailability after oral administration in human, so, 20(R)-Rg3 can be by intranasal administration, the mechanism was related to the increase of the storage of hepatic glycogen, and the decrease of the accumulation of metabolite such as lactic acid and serum urea nitrogen.

Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3β and induction of SHP gene expression, suggests that it has therapeutic potential for type 2 diabetic patients.

Pseudoginsenoside F11, a novel partial PPAR γ agonist, can promote adiponectin oligomerization and secretion in 3T3-L1 adipocytes and inhibit obesity-linked phosphorylation of PPAR γ at Ser-273 by Cdk5. It possesses significant neuroprotective activity, has been demonstrated to antagonize the learning and memory deficits induced by scopolamine, morphine and methamphetamine in mice; it also antagonizes the development of analgesia tolerance to morphine and blocks the development of morphine-induced behavioral sensitization via its effect, at least partially, on the glutamatergic system in the mPFC.

Ginsenoside Rh1 has antiallergic action , may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.

Ginsenoside Rg5 plays a novel role as an IGF-1R agonist, promoting therapeutic angiogenesis and improving hypertension without adverse effects in the vasculature, it can ameliorate lung inflammation possibly by inhibiting the binding of LPS to toll-like receptor (TLR)-4 on macrophages. Ginsenoside Rg5 blocks cell cycle of SK-HEP-1 cells at the Gl/S transition phase by down-regulating cyclin E-dependent kinase activity and that the down-regulation of cyclin E-dependent kinase activity is caused mainly by induced CDK2 inhibitor, p21Cip/WAF1 and decreased levels of cyclin E.

Ginsenoside Rc (Rc), a protopanaxadiol type ginsenoside, is the active component mainly responsible for the therapeutic and pharmacologic properties of ginseng, which are derived from its suppression of superoxide-induced free radicals, Rc can modulate Forkhead box O (FoxO1)phosphorylation through activation of PI3K/Akt and inhibition of AMPK and FoxO1 acetylation through interaction with CBP and SIRT1, and that this leads to upregulation of catalase under conditions of oxidative stress.

Panaxadiol , a ginseng saponin with a dammarane skeleton, selectively interferes with the cell cycle in human cancer cell lines, it inhibits DNA synthesis in a dose-dependent manner with IC50 values ranging from 0.8 to 1.2 μM in SK-HEP-1 cells and HeLa cells, it selectively elevates p21WAF1/CIP1 levels and thereby arrests the cell cycle at G1/S phase by down-regulating Cyclin A-Cdk2 activity.

Ginsenoside Rd (Rd), a saponin isolated from the roots of panax notoginseng, Rd has immunological adjuvant activity, and elicits a Th1 and Th2 immune response by regulating production and gene expression of Th1 cytokines and Th2 cytokines.

Ginsenoside (G)-F1 is an enzymatic metabolite generated from G-Rg1, it has been reported to suppress platelet aggregation and to reduce gap junction-mediated intercellular communication, also as a novel anti-skin cancer drug with anti-proliferative and anti-migration features.

Ginsenoside Re, a main phytosterol of Panax ginseng, inhibits Ca(2+) accumulation in mitochondria during cardiac ischemia/reperfusion, which is attributable to nitric oxide (NO)-induced Ca(2+) channel inhibition and K(+) channel activation in cardiac myocytes, acts as a specific agonist for the nongenomic pathway of sex steroid receptors, and NO released from activated eNOS underlies cardiac K(+) channel activation and protection against ischemia-reperfusion injury, G-Re also exerts antiischemic effect and induces angiogenic regeneration.[1,2]

Ginsenoside-Rg3, possess an ability to inhibit the lung metastasis of tumor cells, and the mechanism of their antimetastatic effect is related to inhibition of the adhesion and invasion of tumor cells, and also to anti-angiogenesis activity.

GinsenosideRf, as an effective natural product, induces G2/Mphase cell cycle arrest and apoptosis in human osteosarcoma MG-63 cells through the mitochondrial pathway, suggests that it may have a therapeutic effect on human osteosarcoma.

Ginsenosides, a class of ginseng compounds of herbal medicine, have therapeutic potential for the neuroprotection of brain damage after cerebral ischemia because of their anti-oxidant and anti-inflammation activities, ginsenoside Rb1 could represent promising applications as anti-oxidants for the anti-aging treatment of neurological disorders, such as stroke, in elderly patients.

Ginsenoside Rb3 has anti-myocardial ischemia-reperfusion injury, neuroprotective, antidepressant-like, and antioxidant effects, it also possesses the potential of the clinical use in preventing and treating diabetes. Ginsenoside Rb3 significantly attenuates the changes of creatine kinase activity and lactate dehydrogenase activity, exhibits inhibitory effect on TNFα-induced NF-κB transcriptional activity with an IC50 of 8.2 μM in 293T cell lines, it also inhibits the induction of COX-2 and iNOS mRNA.

Ginsenoside Rh2 is one of the most active components of red ginseng, controlling cancer and other metabolic diseases including osteoclast differentiation; ginsenoside Rh2 can suppress RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK, it is also suggested to be developed as a therapeutic drug for prevention and treatment of osteoporosis.

Ginsenosides, which are active compounds found in ginseng (Panax ginseng), are used as antidiabetic treatments; ginsenoside Rb2 may inhibit palmitate-induced gluconeogenesis via AMPK-induced SHP by relieving ER stress, a cause of gluconeogenesis.

Ginsenoside Rh3 is a bacterial metabolite of Rg5, which is the main constituent of heat-processed ginseng, has anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.

Ginsenoside Rg1 is the main pharmacologically active compound of ginsenosides and has demonstrated pharmacological effects in the cardiovascular system, central nervous system and immune system; Rg1 has protective effect against Aβ25-35-induced toxicity in PC12 cells,might be through the insulin-like growth factor-I receptor (IGF-IR) and estrogen receptor (ER)signaling pathways.

Ginsenoside Rh2 is one of the most active components of red ginseng, controlling cancer and other metabolic diseases including osteoclast differentiation; ginsenoside Rh2 can suppress RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK, it is also suggested to be developed as a therapeutic drug for prevention and treatment of osteoporosis.

(20R)-Ginsenoside Rh1 exhibits various pharmacological activities including vasorelaxation, antioxidation, anti-inflammation, and anticancer.