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Geniposide
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Product Name Geniposide
Price: $30 / 20mg
CAS No.: 24512-63-8
Catalog No.: CFN98261
Molecular Formula: C17H24O10
Molecular Weight: 388.4 g/mol
Purity: >=98%
Type of Compound: Iridoids
Physical Desc.: Powder
Source: The fruits of Gardenia jasminoides Ellis.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
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Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Geniposide exhibits anti-diabetic, antidepressant-like, antioxidative, anti-apoptotic, antiproliferative and neuroprotective activities. Geniposide is an agonist for GLP-1 receptor, it regulates expression of anti-oxidative proteins including HO-1 and Bcl-2 by activating the transcriptor of p90RSK via MAPK signaling pathway in PC12 cells. Geniposide may suppress TGF-β1-induced EMT in hepatic fibrosis by inhibiting the TGFβ/Smad and ERK-mitogen-activated protein kinase (MAPK) signaling pathways.
Targets: TLR | p53 | Bcl-2/Bax | Caspase | TGF-β/Smad | ERK | p38MAPK | HO-1 | MEK | Raf | Beta Amyloid | BACE | TNF-α | IL Receptor | JNK | ROS | NF-kB | IkB | IKK
In vitro:
Neurochem Int. 2007 Nov-Dec;51(6-7):361-9.
Geniposide, a novel agonist for GLP-1 receptor, prevents PC12 cells from oxidative damage via MAP kinase pathway.[Pubmed: 17629357]
Alzheimer's disease (AD) is the most common form of dementia. Glucagon-like peptide-1 (GLP-1) gives a new genre in therapeutic targets for intervention in AD with its neurotrophic and neuroprotective functions. In previous work, we identified that Geniposide is a novel agonist for GLP-1 receptor, which shows neurotrophic characteristics to induce the neuronal differentiation of PC12 cells.
METHODS AND RESULTS:
The aim of this study is to determine whether Geniposide prevents neurons from oxidative damage, and to explore its signaling pathways. The results demonstrated that Geniposide increased the expression of anti-apoptotic proteins, including Bcl-2 and heme oxygenase-1 (HO-1), to antagonize the oxidative damage in PC12 cells induced by hydrogen peroxide. LY294002 (a PI3K inhibitor) inhibited the effect of Geniposide increasing of Bcl-2 level by activation of MAPK, MEK and c-Raf phosphorylation in hydrogen peroxide treated PC12 cells. U0126 (a selective inhibitor of MEK) also attenuated the enhancement of Geniposide on Bcl-2 level by inhibiting the phosphorylation of p90RSK in the hydrogen peroxide treated PC12 cells.
CONCLUSIONS:
All these data demonstrate that Geniposide, an agonist for GLP-1 receptor, regulates expression of anti-oxidative proteins including HO-1 and Bcl-2 by activating the transcriptor of p90RSK via MAPK signaling pathway in PC12 cells.
Int Immunopharmacol. 2012 Dec;14(4):792-8.
Geniposide, from Gardenia jasminoides Ellis, inhibits the inflammatory response in the primary mouse macrophages and mouse models.[Pubmed: 22878137 ]
Geniposide, a main iridoid glucoside component of gardenia fruit, has been known to exhibit antibacterial, anti-inflammatory and other important therapeutic activities. The objective of this study was to investigate the protective effects of Geniposide on inflammation in lipopolysaccharide (LPS) stimulated primary mouse macrophages in vitro and LPS induced lung injury model in vivo.
METHODS AND RESULTS:
The expression of pro-inflammatory cytokines was determined by enzyme-linked immunosorbent assay (ELISA). Nuclear factor-kappa B (NF-κB), inhibitory kappa B (IκBα) protein, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and Toll-like receptor 4 (TLR4) were determined by Western blot. Further analysis was carried out in mTLR4 and mMD-2 co-transfected HEK293 cells. The results showed that Geniposide markedly inhibited the LPS-induced TNF-α, IL-6 and IL-1β production both in vitro and in vivo. Geniposide blocked the phosphorylation of IκBα, p65, p38, ERK and JNK in LPS stimulated primary mouse macrophages. Furthermore, Geniposide inhibited the expression of TLR4 in LPS stimulated primary mouse macrophages and inhibited the LPS-induced IL-8 production in HEK293-mTLR4/MD-2 cells. In vivo study, it was also observed that Geniposide attenuated lung histopathologic changes in the mouse models.
CONCLUSIONS:
These results suggest that Geniposide exerts an anti-inflammatory property by down-regulating the expression of TLR4 up-regulated by LPS. Geniposide is highly effective in inhibiting acute lung injury and may be a promising potential therapeutic reagent for acute lung injury treatment.
Ethnopharmacol . 2016 Jun 5;185:77-86.
Geniposide attenuates inflammatory response by suppressing P2Y14 receptor and downstream ERK1/2 signaling pathway in oxygen and glucose deprivation-induced brain microvascular endothelial cells[Pubmed: 26976766]
Ethnopharmacological relevance: Fructus gardenia is widely used for treatment of stroke and infectious diseases in Chinese medicine. Geniposide is the key bioactive compound related to the pharmacodynamic actions of gardenia on ischemic stroke. The molecular mechanism by which Geniposide improves the ischemic brain injury was observed in the study. Aim of the study: Recent studies showed that Geniposide had protective activities against the inflammatory response in ischemic stroke. However, the molecular mechanism of Geniposide anti-inflammatory role has not yet been fully elucidated. In this study, we investigated the effect of Geniposide on the expression of P2Y14 receptor and downstream signaling pathway in brain microvascular endothelial cells (BMECs). Materials and methods: An in vitro model of cerebral ischemia in BMECs was established by oxygen-glucose-deprivation (OGD). To further confirm the specific effect of Geniposide on P2Y14 receptor and downstream signaling pathways, we set up a UDP-glucose (an agonist of the P2Y14 receptor) stimulated model. After administration of Geniposide, the expression of P2Y14 receptor, phosphorylation of RAF-1, mitogen activated protein kinase kinase1/2 (MEK1/2), extracellular signal-regulated kinase 1/2 (ERK1/2), level of interleukin-8 (IL-8), interleukin-1β (IL-1β), monocyte chemotactic protein 1 (MCP-1) in BMECs were determined. Results: The mRNA and protein expression of P2Y14 in the rat BMECs were up-regulated in OGD-induced injury. After administration of Geniposide, the expression of P2Y14 receptor was significantly down-regulated, the phosphorylation of RAF-1, MEK1/2, ERK1/2 were suppressed. Similar data were obtained in UDP-glc stimulated model. We also observed that Geniposide markedly declined the production of IL-8, IL-1β and MCP-1 in OGD-induced BMECs. Conclusion: Geniposide exerted anti-inflammatory effects by interfering with the expression of P2Y14 receptor, which subsequently inhibits the downstream ERK1/2 signaling pathways and the release of the pro-inflammatory cytokines IL-8, MCP-1, IL-1β. Therefore, this study provides the evidence for gardenia's clinical application in cerebral ischemia. Keywords: Anti-inflammation; Brain microvascular endothelial cells; ERK1/2 signaling pathway; Geniposide; Geniposide (PubChem CID: 107848); P2Y(14) receptor. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.
In vivo:
Eur Neuropsychopharmacol. 2015 Apr 17.
Antidepressant-like effect of geniposide on chronic unpredictable mild stress-induced depressive rats by regulating the hypothalamus-pituitary-adrenal axis.[Pubmed: 25914157]
Geniposide as the major active component of Gardenia jasminoides Ellis has neuroprotective activity.
METHODS AND RESULTS:
This study elucidated the potential antidepressant-like effect of Geniposide and its related mechanisms using a depression rat model induced by 3 consecutive weeks of chronic unpredictable mild stress (CUMS). Sucrose preference test, open field test (OFT) and forced swimming test (FST) were applied to evaluate the antidepressant effect of Geniposide. We found that Geniposide (25, 50, 100mg/kg) treatment reversed the CUMS-induced behavioral abnormalities, as suggested by increased sucrose intake, improved crossing and rearing behavior in OFT, shortened immobility and prolonged swimming time in FST. Additionally, Geniposide treatment normalized the CUMS-induced hyperactivity of HPA axis, as evidenced by reduced CORT serum level, adrenal gland index and hypothalamic CRH mRNA expression, with no significant effect on ACTH serum level. Moreover, Geniposide treatment upregulated the hypothalamic GRα mRNA level and GRα protein expression in PVN, suggesting Geniposide could recover the impaired GRα negative feedback on CRH expression and HPA axis.
CONCLUSIONS:
These aforementioned therapeutic effects of Geniposide were essentially similar to fluoxetine.
Our results indicated that Geniposide possessed potent antidepressant-like properties that may be mediated by its effects on the HPA axis.
Geniposide Description
Source: The fruits of Gardenia jasminoides Ellis.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.5747 mL 12.8733 mL 25.7467 mL 51.4933 mL 64.3666 mL
5 mM 0.5149 mL 2.5747 mL 5.1493 mL 10.2987 mL 12.8733 mL
10 mM 0.2575 mL 1.2873 mL 2.5747 mL 5.1493 mL 6.4367 mL
50 mM 0.0515 mL 0.2575 mL 0.5149 mL 1.0299 mL 1.2873 mL
100 mM 0.0257 mL 0.1287 mL 0.2575 mL 0.5149 mL 0.6437 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Life Sci. 2014 Dec 5;119(1-2):9-17.
Geniposide inhibited lipopolysaccharide-induced apoptosis by modulating TLR4 and apoptosis-related factors in mouse mammary glands.[Pubmed: 25445441]
Geniposide, a major iridoid glycoside found in gardenia fruit, is widely used in Asian countries for its anti-inflammatory, anti-tumor and anti-apoptotic activities. Although the anti-inflammatory effect of Geniposide has been widely reported, its anti-apoptotic role in mastitis remains unclear. In the present study, we investigated whether Geniposide exerts anti-apoptotic activity in lipopolysaccharide (LPS)-induced mouse mammary glands.
METHODS AND RESULTS:
We established a LPS-induced mouse mastitis model and LPS-stimulated primary mouse mammary epithelial cells (mMECs) model to investigate the anti-apoptotic effect of Geniposide and the underlying mechanism of action.Geniposide alleviated mammary gland apoptosis, down-regulated Bax expression, inhibited Caspase-3 cleavage and p53 phosphorylation and up-regulated Bcl-2 expression in vivo. In vitro, Geniposide decreased the ratio of dead cells in a dose-dependent manner. Geniposide inhibited Bax expression and Caspase-3 cleavage, and up-regulated the expression of Bcl-2. Moreover, Geniposide down-regulated the expression of TLR4 and repressed the phosphorylation of p53.
CONCLUSIONS:
These results demonstrate that the anti-apoptotic property of Geniposide is due to its modulation of TLR4 and apoptosis-related factors (p53, Bax, Bcl-2 and Caspase-3) in LPS-induced mouse mastitis.
Biochimie. 2015 Jun;113:26-34.
Effects of geniposide on hepatocytes undergoing epithelial-mesenchymal transition in hepatic fibrosis by targeting TGFβ/Smad and ERK-MAPK signaling pathways.[Pubmed: 25818617]
Liver fibrosis results from increased deposition of type-I collagen within the hepatic extracellular space and constitutes a common cardinal signature in all forms of liver injury, regardless of etiology. Transforming growth factor β1 (TGF-β1) plays a crucial role in the pathogenesis of liver fibrosis. Geniposide is recognized as being useful against hyperlipidemia and fatty liver. However, its cellular mechanism and anti-fibrotic effect in TGF-β1-induced hepatocytes have not been explored.
METHODS AND RESULTS:
In the present study, we investigated its anti-epithelial-mesenchymal transition (EMT) mechanism by examining the effect of Geniposide on TGF-β1-induced hepatocytes. The effect of Geniposide on TGF-β1-induced AML12 cells was assessed using Western blotting, quantitative real-time PCR, immunofluorescence staining and DNA binding activity. We found that Geniposide significantly inhibited TGF-β1-induced mRNA and protein expression of type-I collagen. Cells treated concurrently with TGF-β1 and Geniposide retained high levels of localized E-cadherin expression with no increase in vimentin. Treatment with Geniposide almost completely blocked the phosphorylation of Smad2/3, extracellular signal-regulated kinase (ERK) and Akt in AML12 cells.
CONCLUSIONS:
Taken together, these results suggest that Geniposide may suppress TGF-β1-induced EMT in hepatic fibrosis by inhibiting the TGFβ/Smad and ERK-mitogen-activated protein kinase (MAPK) signaling pathways. Our results may help researchers better understand the pathogenesis of liver fibrosis so they can develop novel therapeutic strategies for treatment of liver diseases.
Acta Pharmacol Sin. 2010 Aug;31(8):953-62.
Geniposide inhibits high glucose-induced cell adhesion through the NF-kappaB signaling pathway in human umbilical vein endothelial cells.[Pubmed: 20686520 ]
To investigate whether Geniposide, an iridoid glucoside extracted from gardenia jasminoides ellis fruits, inhibits cell adhesion to human umbilical vein endothelial cells (HUVECs) induced by high glucose and its underlying mechanisms.
METHODS AND RESULTS:
HUVECs were isolated from human umbilical cords and cultured. The adhesion of monocytes to HUVECs was determined using fluorescence-labeled monocytes. The mRNA and protein levels of vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) were measured using real-time RT-PCR and ELISA. Reactive oxygen species (ROS) production was measured using a fluorescent probe. The amounts of nuclear factor-kappa B (NF-kappaB) and inhibitory factor of NF-kappaB (IkappaB) were determined using Western blot analysis. The translocation of NF-kappaB from the cytoplasm to the nucleus was determined using immunofluorescence. Geniposide (10-20 mumol/L) inhibited high glucose (33 mmol/L)-induced adhesion of monocytes to HUVECs in a dose-dependent manner. This compound (5-40 mumol/L) also inhibited high glucose-induced expression of VCAM-1 and E-selectin at the gene and protein levels. Furthermore, Geniposide (5-20 micromol/L) decreased ROS production and prevented IkappaB degradation in the cytoplasm and NF-kappaB translocation from the cytoplasm to the nucleus in HUVECs.
CONCLUSIONS:
Geniposide inhibits the adhesion of monocytes to HUVECs and the expression of CAMs induced by high glucose, suggesting that the compound may represent a new treatment for diabetic vascular injury. The mechanism underlying this inhibitory effect may be related to the inhibition of ROS overproduction and NF-kappaB signaling pathway activation by Geniposide.
Animal Research:
Neurochem Int. 2015 Oct;89:7-16.
Geniposide attenuates insulin-deficiency-induced acceleration of β-amyloidosis in an APP/PS1 transgenic model of Alzheimer's disease.[Pubmed: 25882165]
Our previous studies have shown that Geniposide plays an essential role in glucose-stimulated insulin secretion from pancreatic β cells and also antagonizesAβ1-42-induced cytotoxicity examined using a primary cortical neuron assay. However, the mechanism by which Geniposide appears to regulate insulin signaling in the brain is presently not well understood.
METHODS AND RESULTS:
In this study, we administered streptozotocin (STZ) to induce insulin-deficiency in an AD transgenic mouse model, and investigated the effects of Geniposide on the β-amyloidogenic processing of amyloid precursor protein (APP) using in vitro and in vivo models. Our results indicate that treatment with STZ (90 mg/kg, i.p., once daily for two consecutive days) induced significant reduction in peripheral and brain insulin levels in both wild-type and APP/PS1 transgenic mice. Administration of Geniposide for 4 weeks significantly decreased the concentrations of cerebral β-amyloid peptides (Aβ1-40 and Aβ1-42) in STZ-treated AD mice. Further experiments showed that Geniposide up-regulated the protein levels of β-site APP cleaving enzyme (BACE1) and insulin-degrading enzyme (IDE), and decreased the protein levels of ADAM10 when examined using a primary cultured cortical neuron assay and in STZ-induced AD mice. Meanwhile, Geniposide also directly enhanced the effects of insulin by reducing Aβ1-42 levels in primary cultured cortical neurons.
CONCLUSIONS:
Taken together, our findings provide a mechanistic link between diabetes and AD, and is consistent with the notion that Geniposide might play an important role on APP processing via enhancing insulin signaling and may convey a therapeutic benefit in AD.
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