Ginsenoside Rb1

Ginsenoside Rb1 at a Glance

Ginsenoside Rb1 is the dominant protopanaxadiol-type saponin of Asian ginseng, and the compound most often credited with the root’s laboratory signals for neuroprotection, cardioprotection and glucose handling.

The complication with all ginsenosides is metabolic: Rb1 is poorly absorbed and extensively transformed by gut bacteria, largely into compound K, which is what actually circulates. So the molecule studied in vitro is frequently not the molecule present in blood.

Rb1 vs. Rg1: Ginseng’s Two Opposing Saponins

Rb1 and Rg1 are ginseng’s two headline saponins, and they are routinely discussed as a matched pair — which obscures how differently they behave. They sit on opposite sides of one biosynthetic branch point, they end up as different gut metabolites, and in the vasculature they do opposite things.

The chemistry is a single hydroxyl. Rb1 is built on protopanaxadiol (PPD), with two glucoses at C-3 and two at C-20. Rg1 is built on protopanaxatriol (PPT) — the same aglycone plus a hydroxyl at C-6, installed in the plant by one cytochrome P450 acting on protopanaxadiol ^{18Reference 18Han JY et al. · 2012Cytochrome P450 CYP716A53v2 catalyzes the formation of protopanaxatriol from protopanaxadiol during ginsenoside biosynthesis in Panax ginsengView study →}. Ginseng root carries around 43 ginsenosides, sorted into the PPD group Rb1 heads (with Rb2, Rc, Rd), the PPT group (Re, Rf, Rg1), and the oleanane-type Ro ^{21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →}.

	Ginsenoside Rb1	Ginsenoside Rg1
Aglycone class	Protopanaxadiol (PPD)	Protopanaxatriol (PPT)
Sugars	Two glucoses at C-3, two at C-20	Glucose at C-6 and C-20
Richer in	Panax quinquefolius (American)	Panax ginseng (Asian)
In leaf and flower	Present	Absent
Gut end-product	Rd → F2 → compound K	Rh1 → F1 → protopanaxatriol
Angiogenesis	Inhibits (PEDF via ERβ)	Promotes (eNOS, PI3K/Akt)
CNS reputation	Calming	Stimulating
Cholinergic effect	No effect on AChE	Inhibits acetylcholinesterase

The vascular split is the sharpest of the differences. A 2004 Circulation study asked why ginseng extract is credited both with healing wounds and with suppressing tumours, and located the answer in the Rg1:Rb1 ratio, which varies by species and origin. Matrigel implants reconstituted from purified saponins at different ratios behaved accordingly: Rg1 dominance produced angiogenesis, and Rb1 the opposite — it blocked endothelial chemoinvasion, the earliest step ^{13Reference 13Sengupta S et al. · 2004In vitroModulating angiogenesis: the yin and the yang in ginseng — in vivo and in vitroView study →}. The mechanism was later traced to induction of pigment epithelium-derived factor through the oestrogen-β receptor, which suppresses endothelial tube formation ^{14Reference 14Leung KW et al. · 2007In vitroGinsenoside Rb1 inhibits tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor through the oestrogen beta receptor — in vitroView study →}. Rb1 is, in other words, an anti-angiogenic molecule sitting in the same root as a pro-angiogenic one.

Elsewhere the contrast is real but softer. Head to head in scopolamine-impaired mice, both saponins improved memory by different routes: Rg1 was stronger on water-maze acquisition and inhibited acetylcholinesterase, which Rb1 did not; Rb1 was the more effective at restoring hippocampal serotonin ^{16Reference 16Wang Q et al. · 2010AnimalComparison of ginsenosides Rg1 and Rb1 for their effects on improving scopolamine-induced learning and memory impairment in mice — animal modelView study →}. The familiar species-level shorthand — Asian ginseng as the stimulating one because it is Rg1-rich, American ginseng as the calming one because it is Rb1-rich — is drawn from the same asymmetry ^{15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →}, and is better read as a chemotype generalisation than as a property of either molecule.

The metabolic divergence is the one that most changes how the evidence should be read. Both saponins are poorly absorbed and heavily transformed by gut bacteria before anything reaches blood — but into different molecules. Rb1 funnels down to compound K, which has its own pharmacology and its own early human trials; Rg1 does not produce compound K at all, being deglycosylated instead toward Rh1 and F1 ^{11Reference 11Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal modelView study →23Reference 23Odani T et al. · 1983AnimalStudies on the absorption, distribution, excretion and metabolism of ginseng saponinsView study →}. Findings about compound K bear on oral Rb1, and not on oral Rg1.

What It's Used For

Ginsenoside Rb1 is the dominant protopanaxadiol (PPD) saponin of Asian ginseng (Panax ginseng), where it typically sits at around 5.8 mg/g of root and is often the single most abundant ginsenoside present. The relative amount of Rb1 versus the protopanaxatriol saponin ginsenoside Rg1 is one of the chemical fingerprints used to tell the two commercial ginsengs apart: Panax quinquefolius (American ginseng) runs the higher Rb1:Rg1 ratio, Panax ginseng the lower ^{15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →}.

Rb1 carries a very large preclinical literature — neuroprotection in models of cerebral ischemia, cardioprotection against ischemia-reperfusion injury, and effects on glucose uptake and insulin sensitivity — almost all of it in cells or rodents ^{1Reference 1Dong X et al. · 2017AnimalNeuroprotective effects of pretreatment of ginsenoside Rb1 on severe cerebral ischemia-induced injuries in aged mice: involvement of anti-oxidant signaling — mouse, in vivoView study →2Reference 2Liu JW et al. · 2013AnimalEffect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats — rat, in vivo animal modelView study →6Reference 6Li YH et al. · 2016AnimalCardioprotection of ginsenoside Rb1 against ischemia/reperfusion injury is associated with mitochondrial permeability transition pore opening inhibition — rat, in vivo animal modelView study →7Reference 7Wang Z et al. · 2008AnimalGinsenoside Rb1 preconditioning protects against myocardial infarction after regional ischemia and reperfusion by activation of phosphatidylinositol-3-kinase signal transduction — rat, in vivo animal modelView study →8Reference 8Shang WB et al. · 2014In vitroGinsenoside Rb1 upregulates expressions of GLUTs to promote glucose consumption in adipocytes — in vitroView study →9Reference 9Shen L et al. · 2015AnimalGinsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats — rat, in vivo animal modelView study →}.

The critical caveat runs through everything below: isolated Rb1 is barely absorbed when taken by mouth (rat oral bioavailability around 4% or lower), and gut microbiota convert it into compound K, the metabolite that actually reaches the blood in quantity ^{10Reference 10Xu QF et al. · 2003AnimalPharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — rat, in vivo pharmacokineticsView study →11Reference 11Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal modelView study →}.

Ginseng’s clinical reputation rests on whole-extract human data, not on isolated Rb1.

Evidence by IndicationStrength of support · Beta

01Neuroprotection (cerebral ischemia)Shaky40%Multiple rat/mouse stroke models; isolated Rb1; no human trials; poor oral uptake

02CardioprotectionShaky30%Rat/cell ischemia-reperfusion; isolated Rb1; mechanism-level only

03Glucose uptake & insulin sensitivityShaky28%Rat + in vitro adipocyte/muscle; isolated Rb1; no clinical endpoint

04Anti-inflammatory / moodShaky18%Mouse neuroinflammation/depression models; isolated Rb1; thin, indirect

Mechanisms

Pharmacokinetics

Bioavailability is the load-bearing fact for Rb1. Absolute oral bioavailability in rats is very low — on the order of 4.35% in one classic determination, and often cited lower still — because the large, polar saponin is poorly absorbed intact across the gut wall ^{10Reference 10Xu QF et al. · 2003AnimalPharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — rat, in vivo pharmacokineticsView study →}. What reaches the systemic circulation in meaningful quantity is largely its gut-microbiota metabolite: colonic bacteria progressively deglycosylate Rb1 (Rb1 → Rd → F2 → compound K), and compound K is the more absorbable, often more potent active ^{11Reference 11Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal modelView study →}. This microbiota dependence means exposure varies widely between individuals and is blunted by antibiotics; it also reframes the enormous preclinical body, much of which uses injected Rb1 to bypass the gut entirely ^{11Reference 11Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal modelView study →}. Rat work from 1983 made the point for both headline saponins at once, following Rg1 and Rb1 through the digestive tract and finding neither survives it intact ^{23Reference 23Odani T et al. · 1983AnimalStudies on the absorption, distribution, excretion and metabolism of ginseng saponinsView study →}. Circulating Rb1 itself is cleared slowly, with a relatively long terminal half-life reported across rodent studies ^{10Reference 10Xu QF et al. · 2003AnimalPharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — rat, in vivo pharmacokineticsView study →}. The consequences of that conversion — the several-fold between-person variation in compound-K formation, and compound K’s own pharmacology and phase 1 trial — are set out on its own page.

Clinical Trials

There are essentially no registered clinical trials of the isolated compound — human evidence associated with ginsenoside Rb1 comes from whole-Panax ginseng extracts standardized to total ginsenosides, not from Rb1 given alone, so benefits cannot be attributed to Rb1 specifically.

Last checked: September 2026.

Isolate vs. Plant Studies

Everything above is isolated Rb1, and none of it is human. The imbalance is stark: the isolated molecule carries one of the largest preclinical literatures of any plant saponin — stroke models ^{1Reference 1Dong X et al. · 2017AnimalNeuroprotective effects of pretreatment of ginsenoside Rb1 on severe cerebral ischemia-induced injuries in aged mice: involvement of anti-oxidant signaling — mouse, in vivoView study →2Reference 2Liu JW et al. · 2013AnimalEffect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats — rat, in vivo animal modelView study →3Reference 3Cheng Z et al. · 2019ReviewNeuroprotective effects of ginsenosides against cerebral ischemia — reviewView study →4Reference 4Guo Y et al. · 2018AnimalEffects of ginsenoside Rb1 on expressions of phosphorylation Akt/phosphorylation mTOR/phosphorylation PTEN in artificial abnormal hippocampal microenvironment in rats — rat, in vivoView study →}, cardiac ischemia-reperfusion ^{6Reference 6Li YH et al. · 2016AnimalCardioprotection of ginsenoside Rb1 against ischemia/reperfusion injury is associated with mitochondrial permeability transition pore opening inhibition — rat, in vivo animal modelView study →7Reference 7Wang Z et al. · 2008AnimalGinsenoside Rb1 preconditioning protects against myocardial infarction after regional ischemia and reperfusion by activation of phosphatidylinositol-3-kinase signal transduction — rat, in vivo animal modelView study →}, glucose handling ^{8Reference 8Shang WB et al. · 2014In vitroGinsenoside Rb1 upregulates expressions of GLUTs to promote glucose consumption in adipocytes — in vitroView study →9Reference 9Shen L et al. · 2015AnimalGinsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats — rat, in vivo animal modelView study →}, neuroinflammation ^{5Reference 5Zhang L et al. · 2021AnimalGinsenoside Rb1 induces a pro-neurogenic microglial phenotype via PPARγ activation in male mice exposed to chronic mild stress — mouse, animal modelView study →} — while the human ginseng evidence sits entirely at the level of standardised whole-root extract, in which Rb1 is one of forty-odd saponins ^{21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →}. No clinical result belongs to Rb1 specifically.

Two things weaken the step from isolate to plant more than usual. The first is route: a large share of the rodent work injects Rb1, often explicitly to bypass the gut wall that an oral dose must cross. The second is metabolism: an oral dose delivers mostly compound K to the bloodstream, not Rb1 ^{11Reference 11Kang A et al. · 2016AnimalGut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal modelView study →23Reference 23Odani T et al. · 1983AnimalStudies on the absorption, distribution, excretion and metabolism of ginseng saponinsView study →} — so a concentration that inhibits endothelial chemoinvasion in culture is not a concentration a ginseng capsule produces in a person, and the molecule doing the work in vivo may not be Rb1 at all.

The one place the isolate work genuinely explains the plant is the Rg1:Rb1 ratio. Reconstituting ginseng extracts from purified Rg1 and Rb1 at species-typical ratios reproduced the opposite vascular behaviours of the source species ^{13Reference 13Sengupta S et al. · 2004In vitroModulating angiogenesis: the yin and the yang in ginseng — in vivo and in vitroView study →} — isolated-molecule work accounting for a whole-extract observation rather than merely sitting beside it.

Its Role in Plants

Rb1 is the most abundant end-product of a short, well-characterised pathway. Dammarenediol-II synthase cyclises the squalene-derived precursor; CYP716A47 hydroxylates dammarenediol-II to protopanaxadiol, Rb1’s aglycone ^{17Reference 17Han JY et al. · 2011The Cyt P450 enzyme CYP716A47 catalyzes the formation of protopanaxadiol from dammarenediol-II during ginsenoside biosynthesis in Panax ginsengView study →}; glycosyltransferases then hang the sugar chains at C-3 and C-20. A second P450, CYP716A53v2, diverts part of the pool onward to protopanaxatriol and the Rg1 family ^{18Reference 18Han JY et al. · 2012Cytochrome P450 CYP716A53v2 catalyzes the formation of protopanaxatriol from protopanaxadiol during ginsenoside biosynthesis in Panax ginsengView study →} — so Rb1 sits one enzymatic step before the branch, on the trunk of the pathway rather than on a limb of it. In the fresh root much of it exists as malonyl-ginsenoside Rb1, an ester that converts to plain Rb1 only when the root is steamed and dried ^{21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →}.

The ecological function is chemical defence, and Rb1’s family comes off worse at it than Rg1’s. Tested against six fungi, the PPD fraction inhibited five ginseng non-pathogens — but against Cylindrocarpon destructans, the fungus that causes ginseng root rot, the PPD fraction significantly enhanced the pathogen’s growth, while the PPT fraction inhibited it ^{19Reference 19Zhao X et al. · 2012In vitroFungal sensitivity to and enzymatic deglycosylation of ginsenosides — in vitroView study →}. The reason is enzymatic: the pathogen secretes glycosidases that strip sugars from the C-3 and C-20 chains of PPD-type ginsenosides, converting Rb1 and its relatives into gypenoside XVII, compounds O and Mb, and ginsenoside F2 ^{19Reference 19Zhao X et al. · 2012In vitroFungal sensitivity to and enzymatic deglycosylation of ginsenosides — in vitroView study →}. That is the same stepwise deglycosylation the human gut microbiota performs on the way to compound K — here operating as a virulence factor rather than a bioactivation.

Anatomically Rb1 is less restricted than its sibling. In Panax notoginseng, the underground organs carry both saponin families, and the leaf and flower carry protopanaxadiol-type saponins only — so Rb1’s class is present in the aerial parts where Rg1’s is absent, with Rc, Rb2 and Rb3 (rare underground) especially concentrated there. No saponin at all is detectable in the seed ^{20Reference 20Wan JB et al. · 2006Chemical characteristics for different parts of Panax notoginseng using pressurized liquid extraction and HPLC-ELSDView study →}.

Prevalence in Nature

Rb1 is confined to Panax (Araliaceae). Within the genus it is usually the single most abundant ginsenoside, and it is the molecule the American/Asian distinction turns on: Panax quinquefolius carries more Rb1, Re and Rd than P. ginseng, which is comparatively richer in Rg1, Rb2 and Rc — so the Rb1:Rg1 ratio is high in American ginseng and low in Asian ^{15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →}. Panax notoginseng is richer in total ginsenosides than either, roughly twice white American ginseng and five times white Asian ginseng ^{22Reference 22Sun S et al. · 2011In vitroRed notoginseng: higher ginsenoside content and stronger anticancer potential than Asian and American ginseng — in vitroView study →}.

Processing moves the number as much as species does. Korean red ginseng is regulated on a combined marker of ginsenosides Rb1, Rg1 and Rg3 of 2.5–34 mg/g — an eleven-fold permitted range, which is the real scale of variation in commercial material ^{21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →}. Steaming to make red ginseng lowers Rb1 along with Rg1, Re, Rc and Rd while raising the less polar Rg2, Rh1 and Rg3; the anticancer-studied Rh2 is itself obtained from Rb1 by steaming ^{15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →}. A red-ginseng product therefore contains less Rb1 and more of Rb1’s degradation products than the white root it was made from.

Major Natural Sources

Source	Part	Rb1 status
American ginseng (Panax quinquefolius)	Root	The Rb1-rich ginseng — higher Rb1, Re and Rd than Asian ginseng 15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →
Asian ginseng (Panax ginseng)	Root	Usually the most abundant single ginsenoside present, but at a lower Rb1:Rg1 ratio than American 15Reference 15Chen CF et al. · 2008ReviewComparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — reviewView study →21Reference 21So SH et al. · 2018ReviewRed ginseng monograph — reviewView study →
Notoginseng (Panax notoginseng)	Root, rhizome	Highest total ginsenoside content of the three commercial ginsengs 22Reference 22Sun S et al. · 2011In vitroRed notoginseng: higher ginsenoside content and stronger anticancer potential than Asian and American ginseng — in vitroView study →
Notoginseng	Leaf, flower	Protopanaxadiol saponins only — Rb1’s class, with Rc, Rb2 and Rb3 enriched 20Reference 20Wan JB et al. · 2006Chemical characteristics for different parts of Panax notoginseng using pressurized liquid extraction and HPLC-ELSDView study →
Notoginseng	Seed	No saponins detected 20Reference 20Wan JB et al. · 2006Chemical characteristics for different parts of Panax notoginseng using pressurized liquid extraction and HPLC-ELSDView study →

Discovery & Synthesis

Rb1’s structure was established in 1974 by Syuichi Sanada, Noriko Kondo, Junzo Shoji, Osamu Tanaka and Shoji Shibata, in “Studies on the Saponins of Ginseng. I” — the paper that settled Ro, Rb1, Rb2, Rc and Rd together ^{24Reference 24Sanada S et al. · 1974Studies on the saponins of ginsengView study →}. It came out of the same Tokyo programme that had fixed the structure of the protopanaxatriol saponin Rg1 six years earlier, and it is where the family’s odd naming convention comes from: R for the root, then a letter-and-subscript index assigned by chromatographic mobility rather than by discovery or importance. Rb1 and Rg1 have adjacent-sounding names because their spots landed near each other on a thin-layer plate, not because they are chemically close.

The metabolic half of the story followed in the same country, in a long Chemical and Pharmaceutical Bulletin series through the early 1980s that traced what becomes of Rb1 and Rg1 in the rat gut — the work that first showed the parent saponins do not survive digestion ^{23Reference 23Odani T et al. · 1983AnimalStudies on the absorption, distribution, excretion and metabolism of ginseng saponinsView study →}.

There is no commercially relevant total synthesis of Rb1. It is a dammarane triterpene bearing four sugars and defined stereochemistry at C-20; extraction from Panax root is far cheaper, and commercial Rb1 is isolated by solvent extraction and chromatography. The live alternative is biotechnological — the pathway genes have been moved into heterologous hosts, where PgDDS with CYP716A47 yields protopanaxadiol in transgenic tobacco and rice ^{17Reference 17Han JY et al. · 2011The Cyt P450 enzyme CYP716A47 catalyzes the formation of protopanaxadiol from dammarenediol-II during ginsenoside biosynthesis in Panax ginsengView study →}. A second industrial route runs the other way, using enzymes or fermentation to convert Rb1 into the rarer, more absorbable downstream saponins, chiefly compound K and Rg3.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

Ginsenoside Rb1 is regarded as low in toxicity at the levels supplied by normal ginseng use, and it is one of the best-tolerated ginsenosides in animal work ^{3Reference 3Cheng Z et al. · 2019ReviewNeuroprotective effects of ginsenosides against cerebral ischemia — reviewView study →}. The main practical cautions attach to whole ginseng rather than the isolated saponin: possible additive effects on blood glucose (relevant alongside anti-diabetic drugs, given Rb1’s insulin-sensitizing signal) ^{9Reference 9Shen L et al. · 2015AnimalGinsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats — rat, in vivo animal modelView study →}, and the general ginseng cautions around stimulation and anticoagulant/antiplatelet interactions. The one specific isolated-Rb1 safety signal worth flagging is developmental: in a whole-rat-embryo culture model, Rb1 was teratogenic to rat embryos at high concentrations in vitro ^{12Reference 12Chan LY et al. · 2003In vitroAn in-vitro study of ginsenoside Rb1-induced teratogenicity using a whole rat embryo culture model — in vitroView study →}. This is an in-vitro finding at supraphysiologic exposure, not evidence of harm from dietary ginseng.

Dosage

There is no established human dose for isolated ginsenoside Rb1; it is a research compound, not a standardized supplement. For orientation only, the preclinical exposures cited above were rodent doses — for example cerebral-ischemia rat studies used roughly 20–80 mg/kg of Rb1 by injection ^{2Reference 2Liu JW et al. · 2013AnimalEffect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats — rat, in vivo animal modelView study →}, and metabolic rat studies used short courses of oral Rb1 ^{9Reference 9Shen L et al. · 2015AnimalGinsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats — rat, in vivo animal modelView study →} — routes and doses chosen partly to work around Rb1’s poor oral absorption. None of these translate directly to a human oral dose, and human ginseng intake is taken as whole standardized extract, not isolated Rb1. These are doses studied in research and are not a personal recommendation.

References

1. Dong X, Zheng L, Lu S, Yang Y, et al. (2017). Neuroprotective effects of pretreatment of ginsenoside Rb1 on severe cerebral ischemia-induced injuries in aged mice: involvement of anti-oxidant signaling — mouse, in vivo. Geriatrics & Gerontology International. https://pubmed.ncbi.nlm.nih.gov/26712031/
2. Liu JW, Ren YL, Liu XL, et al. (2013). Effect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats — rat, in vivo animal model. Chinese Journal of Integrated Traditional and Western Medicine. https://pubmed.ncbi.nlm.nih.gov/24517072/
3. Cheng Z, Zhang M, Ling C, et al. (2019). Neuroprotective effects of ginsenosides against cerebral ischemia — review. Molecules. https://pubmed.ncbi.nlm.nih.gov/30897756/
4. Guo Y, Wang LP, Li C, et al. (2018). Effects of ginsenoside Rb1 on expressions of phosphorylation Akt/phosphorylation mTOR/phosphorylation PTEN in artificial abnormal hippocampal microenvironment in rats — rat, in vivo. Neurochemical Research. https://pubmed.ncbi.nlm.nih.gov/30167941/
5. Zhang L, et al. (2021). Ginsenoside Rb1 induces a pro-neurogenic microglial phenotype via PPARγ activation in male mice exposed to chronic mild stress — mouse, animal model. Journal of Neuroinflammation. https://pubmed.ncbi.nlm.nih.gov/34372875/
6. Li YH, et al. (2016). Cardioprotection of ginsenoside Rb1 against ischemia/reperfusion injury is associated with mitochondrial permeability transition pore opening inhibition — rat, in vivo animal model. Chinese Journal of Integrative Medicine. https://pubmed.ncbi.nlm.nih.gov/26740222/
7. Wang Z, et al. (2008). Ginsenoside Rb1 preconditioning protects against myocardial infarction after regional ischemia and reperfusion by activation of phosphatidylinositol-3-kinase signal transduction — rat, in vivo animal model. Cardiovascular Drugs and Therapy. https://pubmed.ncbi.nlm.nih.gov/18679782/
8. Shang WB, et al. (2014). Ginsenoside Rb1 upregulates expressions of GLUTs to promote glucose consumption in adipocytes — in vitro. China Journal of Chinese Materia Medica. https://pubmed.ncbi.nlm.nih.gov/25850283/
9. Shen L, Haas M, Wang DQ, et al. (2015). Ginsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats — rat, in vivo animal model. Physiological Reports. https://pubmed.ncbi.nlm.nih.gov/26359241/
10. Xu QF, Fang XL, Chen DF (2003). Pharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats — rat, in vivo pharmacokinetics. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/12648814/
11. Kang A, Zhang S, Zhu D, et al. (2016). Gut microbiota in the pharmacokinetics and colonic deglycosylation metabolism of ginsenoside Rb1 in rats: contrary effects of antimicrobials treatment and restraint stress — rat, in vivo animal model. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/27613481/
12. Chan LY, Chiu PY, Lau TK (2003). An in-vitro study of ginsenoside Rb1-induced teratogenicity using a whole rat embryo culture model — in vitro. Human Reproduction. https://pubmed.ncbi.nlm.nih.gov/14507839/
13. Sengupta S, Toh SA, Sellers LA, et al. (2004). Modulating angiogenesis: the yin and the yang in ginseng — in vivo and in vitro. Circulation. https://pubmed.ncbi.nlm.nih.gov/15337705/
14. Leung KW, Cheung LW, Pon YL, et al. (2007). Ginsenoside Rb1 inhibits tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor through the oestrogen beta receptor — in vitro. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/17603552/
15. Chen CF, Chiou WF, Zhang JT (2008). Comparison of the pharmacological effects of Panax ginseng and Panax quinquefolium — review. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/18718179/
16. Wang Q, Sun LH, Jia W, et al. (2010). Comparison of ginsenosides Rg1 and Rb1 for their effects on improving scopolamine-induced learning and memory impairment in mice — animal model. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/20564503/
17. Han JY, Kim HJ, Kwon YS, et al. (2011). The Cyt P450 enzyme CYP716A47 catalyzes the formation of protopanaxadiol from dammarenediol-II during ginsenoside biosynthesis in Panax ginseng. Plant and Cell Physiology. https://pubmed.ncbi.nlm.nih.gov/22039120/
18. Han JY, Hwang HS, Choi SW, et al. (2012). Cytochrome P450 CYP716A53v2 catalyzes the formation of protopanaxatriol from protopanaxadiol during ginsenoside biosynthesis in Panax ginseng. Plant and Cell Physiology. https://pubmed.ncbi.nlm.nih.gov/22875608/
19. Zhao X, Gao J, Song C, et al. (2012). Fungal sensitivity to and enzymatic deglycosylation of ginsenosides — in vitro. Phytochemistry. https://pubmed.ncbi.nlm.nih.gov/22449289/
20. Wan JB, Yang FQ, Li SP, et al. (2006). Chemical characteristics for different parts of Panax notoginseng using pressurized liquid extraction and HPLC-ELSD. Journal of Pharmaceutical and Biomedical Analysis. https://pubmed.ncbi.nlm.nih.gov/16522361/
21. So SH, Lee JW, Kim YS, et al. (2018). Red ginseng monograph — review. Journal of Ginseng Research. https://pubmed.ncbi.nlm.nih.gov/30337816/
22. Sun S, Qi LW, Du GJ, et al. (2011). Red notoginseng: higher ginsenoside content and stronger anticancer potential than Asian and American ginseng — in vitro. Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/21344064/
23. Odani T, Tanizawa H, Takino Y (1983). Studies on the absorption, distribution, excretion and metabolism of ginseng saponins. IV. Decomposition of ginsenoside-Rg1 and -Rb1 in the digestive tract of rats — animal model. Chemical and Pharmaceutical Bulletin. https://doi.org/10.1248/cpb.31.3691
24. Sanada S, Kondo N, Shoji J, et al. (1974). Studies on the saponins of ginseng. I. Structures of ginsenoside-Ro, -Rb1, -Rb2, -Rc and -Rd. Chemical and Pharmaceutical Bulletin. https://doi.org/10.1248/cpb.22.421

View all 24 references▾