Ampelopsin

CAS# 27200-12-0

Ampelopsin

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Chemical structure

Ampelopsin

3D structure

Chemical Properties of Ampelopsin

Cas No. 27200-12-0 SDF Download SDF
PubChem ID 161557 Appearance White-pale yellow powder
Formula C15H12O8 M.Wt 320.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms Ampeloptin; Ampelopsin
Solubility DMSO : ≥ 100 mg/mL (312.26 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name (2R,3R)-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydrochromen-4-one
SMILES C1=C(C=C(C(=C1O)O)O)C2C(C(=O)C3=C(C=C(C=C3O2)O)O)O
Standard InChIKey KJXSIXMJHKAJOD-LSDHHAIUSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Ampelopsin

1 Larix sp. 2 Mahonia sp. 3 Pinus sp. 4 Salix sp. 5 Syzygium sp.

Biological Activity of Ampelopsin

DescriptionAmpelopsin,a major antifungal constituent from Salix sachalinensis, which has hepatoprotective, anti-inflammatory,antioxidant, antitumor, anti-invasive and anti-metastatic effects. It is an effective mTOR inhibitor, it inhibited the interconnected ROS/Akt/IKK/NF-κB signaling pathways, and it inhibited H₂O₂-induced apoptosis by ERK and Akt signaling pathways and up-regulation of heme oxygenase-1.
TargetsTNF-α | IL Receptor | NO | NF-kB | NOS | Akt | PI3K | IkB | MAPK | ROS | Bcl-2/Bax | Caspase | ROS | HO-1 | ERK | mTOR | P-gp | Antifection | IKK
In vitro

Ampelopsin reduces endotoxic inflammation via repressing ROS-mediated activation of PI3K/Akt/NF-κB signaling pathways.[Pubmed: 22193240 ]

Int Immunopharmacol. 2012 Jan;12(1):278-87.

Ampelopsin (AMP), a plant flavonoid, has potent anti-inflammatory properties in vitro and in vivo. The molecular mechanisms of Ampelopsin on pharmacological and biochemical actions of RAW264.7 macrophages in inflammation have not been clearly elucidated yet.
METHODS AND RESULTS:
In the present study, non-cytotoxic level of Ampelopsin significantly inhibited the release of nitric oxide (NO) and pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α in a dose-dependent manner. Consistent with NO inhibition, Ampelopsin suppressed lipopolysaccharide (LPS)-induced expression of inducible NO synthase (iNOS) by inhibiting nuclear factor κB (NF-κB) activation, which highly correlated with its inhibitory effect on IκB kinase (IKK) phosphorylation, IκB phosphorylation and NF-κB nuclear translocation. Further study demonstrated that Ampelopsin suppressed LPS-induced activation of Akt without effecting mitogen-activated protein kinases (MAPKs) phosphorylation. A pharmacological inhibitor of the phosphoinositide 3-kinase (PI3K)-Akt pathway, LY294002, abrogated IKK/IκB/NF-κB-mediated iNOS gene expression. Finally, we certificated that Ampelopsin reduced reactive oxygen species (ROS) accumulation and an anti-oxidant N-acetyl-L-cysteine (NAC) significantly repressed LPS-induced PI3K/Akt phosphorylation and the downstream IKK/IκB activation. NAC thereby inhibited LPS-induced iNOS expression and NO production.
CONCLUSIONS:
The present results suggest that the anti-inflammatory effect of Ampelopsin is due to inhibiting the interconnected ROS/Akt/IKK/NF-κB signaling pathways.

Ampelopsin, a Major Antifungla Constitutent from Salix sachalinensis, and its Methyl Ethers.[Reference: WebLink]

Journal of the Agricultural Chemical Society of Japan, 2001, 75(6):659-67.


METHODS AND RESULTS:
To measure the antifungal potency of plant secondary metabolites, we did an antifungal test using Cladosporium herbarum as a test fungus and minute extracts of some plants. This test showed that the methanol extract of Salix sachalinensis leaves had strong antifungal activity. An antifugal principle in the leaves has been identified as (2R,3R)-(+)-5,7,3 ' ,4 ' ,5 ' -pentahydroxy-dihydroflavonol (Ampelopsin). The antifungal potency of S. sachalinensis leaves was not due to an antifungal constituent with high specific activity, but due to the high content of Ampelopsin.
CONCLUSIONS:
To improve the antifungal activity, Ampelopsin was made into variously methylated derivatives, and these products were bioassayed. 7,3 ' ,4 ' -Tri-O-methylAmpelopsin, out of 8 derivatives, had the strongest antifungal activity, which was about 4 times that of Ampelopsin. The structure-activity relationship is briefly discussed.

In vivo

Hepatoprotective activity of tocha, the stems and leaves of Ampelopsis grossedentata, and ampelopsin.[Pubmed: 15630194]

Biofactors. 2004;21(1-4):175-8.


METHODS AND RESULTS:
Hepatoprotective effect of the leaves and stems of Ampelopsis grossedentata together with its main constituent, Ampelopsin, were examined on D-galactosamine induced liver injury in rats. The diet containing 50% ethanolic extract (1%) and Ampelopsin (0.1%) markedly suppressed the increase of LDH, ALT, AST, alpha-tocopherol levels and GSG/GSSH caused by GalN treatment.
CONCLUSIONS:
These results suggested that Ampelopsin from Tocha acted to prevent the oxidative stress in vivo that may have been due to active oxygen species formed by a macrophage by the action of GalN.

Ampelopsin suppresses breast carcinogenesis by inhibiting the mTOR signalling pathway.[Pubmed: 24861637]

Carcinogenesis. 2014 Aug;35(8):1847-54.

The mammalian target of rapamycin (mTOR), which is a master regulator of cellular catabolism and anabolism, plays an important role in tumourigenesis and progression.
METHODS AND RESULTS:
In this study, we report the chemopreventive effect of the dietary compound Ampelopsin (AMP) on breast carcinogenesis in vivo and in vitro, which acts by inhibiting the mTOR signalling pathway. Our study indicates that AMP treatment effectively suppresses 1-methyl-1-nitrosourea (MNU)-induced breast carcinogenesis in rats and inhibits 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and benzo[a]pyrene (B[a]P)-induced cellular carcinogenesis. Additionally, AMP inhibits the growth of breast cancer cells in vitro and in vivo. The activity of mTOR kinase was found to be significantly increased in a time-dependent manner during chronic breast carcinogenesis, and this increase can be suppressed by AMP co-treatment. AMP also effectively suppresses mTOR activity in breast cancer MDA-MB-231 cells. We also demonstrated that AMP is an effective mTOR inhibitor that binds to one site on the mTOR target in two ways. Further studies confirmed that AMP inhibits the activation of Akt, suppresses the formation of mTOR complexes (mTORC)1/2 by dissociating regulatory-associated protein of mTOR and rapamycin-insensitive companion of mTOR and, consequently, decreases the activation of the downstream targets of mTOR, including ribosomal p70-S6 kinase, ribosomal protein S6, eukaryotic translation initiation factor 4B and eukaryotic translation initiation factor 4E-binding protein 1.
CONCLUSIONS:
These finding suggest that AMP is a bioactive natural chemopreventive agent against breast carcinogenesis and is an effective mTOR inhibitor that may be developed as a useful chemotherapeutic agent in the treatment of breast cancer.

Protocol of Ampelopsin

Cell Research

Ampelopsin inhibits H₂O₂-induced apoptosis by ERK and Akt signaling pathways and up-regulation of heme oxygenase-1.[Pubmed: 22144097]

Ampelopsin induces apoptosis via altering expression of Bcl-2/Bax and activating caspase-3 in human hepatoma cell line Bel-7402.[Reference: WebLink]

Chinese Pharmacological Bulletin, 2009, 25(11):1502-6.

To investigate the effects of Ampelopsin on induction of apoptosis in human hepatocellular carcinoma Bel-7402 cells.
METHODS AND RESULTS:
Bel-7402 cells were treated with Ampelopsin with different concentrations for 24,48 and 72 h. The cell proliferation was detected by MTT assay. The morphological change of cells was observed through microscope observation by fluorescence staining. DNA fragmentation was visualized by agarose gel electrophoresis. The apoptosis rate was analyzed by flow cytometry. The expressions of caspase-3, Bcl-2 and Bax protein were detected by Western blot. Ampelopsin inhibited the proliferation of Bel7402 cell line in a dose-and time-dependent manner. The IC50 values were 89.6 ± 16.1, 36.2 ± 6.5 and 15.3 ± 3.0 mg·L-1 at 24,48 and 72 h, respectively. The fluorescence microscope showed clearly cell apoptosis with apoptotic body. Agarose gel electrophoresis result showed that Bel-7402 treated with Ampelopsin produced a DNA ladder band. The sub-G1 peak was detected and resulted in dose-and time-dependent increasing of the population of sub-G1 DNA content by flow cytometry. The expression of Bcl-2 protein was down-regulated, while the expression of Bax protein was up-regulated. The pro-caspase-3 protein was down-expressed and activated.
CONCLUSIONS:
Ampelopsin could inhibit Bel-7402 proliferation through inducing cell apoptosis. The mechanism might be that Ampelopsin could directly or indirectly enhance the level of anti-apoptosis protein Bcl-2 and decrease the level of apoptosis protein Bax. The pathway of pro-caspase-3 activated was initiated and effector caspase-3 was sequentially activated.

Phytother Res. 2012 Jul;26(7):988-94.

Oxidative stress plays an important role in neurodegenerative disorders. Ampelopsin, a flavonoid abundant in Rattan tea (Ampelopsis grossedentata), is a potent antioxidant and its neuroprotective effect against H₂O₂-induced apoptosis in PC12 cells is investigated here for the first time.
METHODS AND RESULTS:
It was found that treatment of cells with Ampelopsin for 1 h significantly reduced the loss of vitality, LDH release and apoptosis and inhibited the formation of reactive oxygen species (ROS). Ampelopsin was able to prevent the activation of p38 induced by H₂O₂. In addition, up-regulation of heme oxygenase-1 (HO-1) expression by Ampelopsin was shown to be both dose- and time-dependent. Mechanically, HO-1 expression induced by Ampelopsin was found to be due to activation of the ERK and Akt signaling pathways, because it was almost completely blocked by the specific inhibitors of ERK and Akt.
CONCLUSIONS:
These results suggest that Ampelopsin increases cellular antioxidant defense through activation of the ERK and Akt signaling pathways, which induces HO-1 expression and thereby protects PC12 cells from H₂O₂-induced apoptosis.

Animal Research

Ampelopsin sodium exhibits antitumor effects against bladder carcinoma in orthotopic xenograft models.[Pubmed: 22241170 ]

Anticancer Drugs. 2012 Jul;23(6):590-6.

The aim of this study was to establish xenograft models of tumor in mice bladder and evaluate the antitumor efficacy of Ampelopsin sodium (Amp-Na).
CONCLUSIONS:
A total of 2×10 human bladder carcinoma EJ cells and murine sarcoma 180 cells were instilled into the bladder of BALB/c nu/nu mice and Swiss mice after preconditioning to establish the tumor model. Mice bearing orthotopic tumors were treated with Amp-Na by intravenous, intraperitoneal, or intravesical instillation. In addition, the pharmacokinetics property of Amp-Na was investigated in normal BALB/c mice. Our results showed that Amp-Na was excreted mainly through the urine, where it existed at a high concentration. Amp-Na significantly inhibited the proliferation of EJ and sarcoma 180 cells both in vivo and in vitro and this can be at least partially attributed to the cell cycle arrest induced by Amp-Na.
CONCLUSIONS:
This study suggests that the use of Amp-Na is an attractive chemotherapeutic modality for bladder cancer patients.

Ampelopsin Dilution Calculator

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Preparing Stock Solutions of Ampelopsin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.1221 mL 15.6104 mL 31.2207 mL 62.4415 mL 78.0518 mL
5 mM 0.6244 mL 3.1221 mL 6.2441 mL 12.4883 mL 15.6104 mL
10 mM 0.3122 mL 1.561 mL 3.1221 mL 6.2441 mL 7.8052 mL
50 mM 0.0624 mL 0.3122 mL 0.6244 mL 1.2488 mL 1.561 mL
100 mM 0.0312 mL 0.1561 mL 0.3122 mL 0.6244 mL 0.7805 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Ampelopsin

Dihydromyricetin is a potent inhibitor with an IC50 of 48 μM on dihydropyrimidinase. Dihydromyricetin can activate autophagy through inhibiting mTOR signaling. Dihydromyricetin suppresses the formation of mTOR complexes (mTORC1/2).

In Vitro:Dihydromyricetin, a flavonol, significantly inhibits the catalytic activities of dihydropyrimidinase toward both the natural substrate dihydrouracil and xenobiotic substrate 5-propyl-hydantoin. Dihydromyricetin exhibits a significant inhibitory effect on the activities of dihydropyrimidinase for both substrates, even more than Myricetin does. The IC50 values of Dihydromyricetin for dihydropyrimidinase determined from the titration curves using Dihydrouracil and 5-propyl-hydantoin are 48±2 and 40±2 μM, respectively[1]. Dihydromyricetin (DHM) supplementation significantly reverses the increased phosphorylation of mTOR at Ser2448 (p-mTOR) during D-gal administration, which suggests that Dihydromyricetin can activate autophagy through inhibiting mTOR signaling[2].

In Vivo:Changes in learning and memory capacity in rats administrated normal control group, D-gal group, D-gal+Dihydromyricetin (100 mg/kg) group, D-gal+Dihydromyricetin (200 mg/kg) group assessed by morris water maze (MWM) (n=10 per group). Dihydromyricetin (DHM) treatment significantly shortens the escape latency when compared with D-gal-induced model group[2].

References:
[1]. Huang CY. Inhibition of a Putative Dihydropyrimidinase from Pseudomonas aeruginosa PAO1 by Flavonoids and Substrates of Cyclic Amidohydrolases. PLoS One. 2015 May 19;10(5):e0127634. [2]. Kou X, et al. Ampelopsin attenuates brain aging of D-gal-induced rats through miR-34a-mediated SIRT1/mTORsignal pathway. Oncotarget. 2016 Nov 15;7(46):74484-74495. [3]. Chang H, et al. Ampelopsin suppresses breast carcinogenesis by inhibiting the mTOR signalling pathway. Carcinogenesis. 2014 Aug;35(8):1847-54.

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References on Ampelopsin

Ampelopsin sodium exhibits antitumor effects against bladder carcinoma in orthotopic xenograft models.[Pubmed:22241170]

Anticancer Drugs. 2012 Jul;23(6):590-6.

The aim of this study was to establish xenograft models of tumor in mice bladder and evaluate the antitumor efficacy of Ampelopsin sodium (Amp-Na). A total of 2x10 human bladder carcinoma EJ cells and murine sarcoma 180 cells were instilled into the bladder of BALB/c nu/nu mice and Swiss mice after preconditioning to establish the tumor model. Mice bearing orthotopic tumors were treated with Amp-Na by intravenous, intraperitoneal, or intravesical instillation. In addition, the pharmacokinetics property of Amp-Na was investigated in normal BALB/c mice. Our results showed that Amp-Na was excreted mainly through the urine, where it existed at a high concentration. Amp-Na significantly inhibited the proliferation of EJ and sarcoma 180 cells both in vivo and in vitro and this can be at least partially attributed to the cell cycle arrest induced by Amp-Na. This study suggests that the use of Amp-Na is an attractive chemotherapeutic modality for bladder cancer patients.

Ampelopsin suppresses breast carcinogenesis by inhibiting the mTOR signalling pathway.[Pubmed:24861637]

Carcinogenesis. 2014 Aug;35(8):1847-54.

The mammalian target of rapamycin (mTOR), which is a master regulator of cellular catabolism and anabolism, plays an important role in tumourigenesis and progression. In this study, we report the chemopreventive effect of the dietary compound Ampelopsin (AMP) on breast carcinogenesis in vivo and in vitro, which acts by inhibiting the mTOR signalling pathway. Our study indicates that AMP treatment effectively suppresses 1-methyl-1-nitrosourea (MNU)-induced breast carcinogenesis in rats and inhibits 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and benzo[a]pyrene (B[a]P)-induced cellular carcinogenesis. Additionally, AMP inhibits the growth of breast cancer cells in vitro and in vivo. The activity of mTOR kinase was found to be significantly increased in a time-dependent manner during chronic breast carcinogenesis, and this increase can be suppressed by AMP co-treatment. AMP also effectively suppresses mTOR activity in breast cancer MDA-MB-231 cells. We also demonstrated that AMP is an effective mTOR inhibitor that binds to one site on the mTOR target in two ways. Further studies confirmed that AMP inhibits the activation of Akt, suppresses the formation of mTOR complexes (mTORC)1/2 by dissociating regulatory-associated protein of mTOR and rapamycin-insensitive companion of mTOR and, consequently, decreases the activation of the downstream targets of mTOR, including ribosomal p70-S6 kinase, ribosomal protein S6, eukaryotic translation initiation factor 4B and eukaryotic translation initiation factor 4E-binding protein 1. These finding suggest that AMP is a bioactive natural chemopreventive agent against breast carcinogenesis and is an effective mTOR inhibitor that may be developed as a useful chemotherapeutic agent in the treatment of breast cancer.

[Reversal effect and its mechanism of ampelopsin on multidrug resistance in K562/ADR cells].[Pubmed:19624024]

Zhongguo Zhong Yao Za Zhi. 2009 Mar;34(6):761-5.

OBJECTIVE: To investigate the inhibitory effect of Ampelopsin (AMP) combined with adriamycin (ADR) on growth of human leukemia multidrug resistant cell line K562/ADR. METHOD: MTT assay was used to detect the effect of AMP on the cytotoxicity of ADR. Jin's formula was used to analyze the effect of combined drug therapy. The expression of P-glycoprotein (P-gp) on cell membrane of K562/ADR was detected using PE-labeled antibody. Flow cytometry was used to determine the influence of AMP on the intracellular accumulation of ADR. RESULT: AMP at the concentration of 1.25 to 5 mg x L(-1) could significantly reverse the multidrug resistance (MDR) to ADR in K562/ADR cells. Co-administration of 1.25 mg x L(-1) AMP and low concentrations of ADR showed an antagonistic effect, while there was an additional to synergistic effect when the concentration of AMP was above 2.5 mg x L(-1). AMP could decrease the expression of P-gp in a concentration-dependent manner and increase the intracellular accumulation of ADR in K562/ADR cells. CONCLUSION: AMP could increased the cytotoxicity and the intracellular accumulation of chemotherapeutic drugs in MDR associated tumor cells through inhibiting the efflux of drugs by P-gp. AMP may be a promising MDR modulator.

Ampelopsin reduces endotoxic inflammation via repressing ROS-mediated activation of PI3K/Akt/NF-kappaB signaling pathways.[Pubmed:22193240]

Int Immunopharmacol. 2012 Jan;12(1):278-87.

Ampelopsin (AMP), a plant flavonoid, has potent anti-inflammatory properties in vitro and in vivo. The molecular mechanisms of Ampelopsin on pharmacological and biochemical actions of RAW264.7 macrophages in inflammation have not been clearly elucidated yet. In the present study, non-cytotoxic level of Ampelopsin significantly inhibited the release of nitric oxide (NO) and pro-inflammatory cytokines such as interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha in a dose-dependent manner. Consistent with NO inhibition, Ampelopsin suppressed lipopolysaccharide (LPS)-induced expression of inducible NO synthase (iNOS) by inhibiting nuclear factor kappaB (NF-kappaB) activation, which highly correlated with its inhibitory effect on IkappaB kinase (IKK) phosphorylation, IkappaB phosphorylation and NF-kappaB nuclear translocation. Further study demonstrated that Ampelopsin suppressed LPS-induced activation of Akt without effecting mitogen-activated protein kinases (MAPKs) phosphorylation. A pharmacological inhibitor of the phosphoinositide 3-kinase (PI3K)-Akt pathway, LY294002, abrogated IKK/IkappaB/NF-kappaB-mediated iNOS gene expression. Finally, we certificated that Ampelopsin reduced reactive oxygen species (ROS) accumulation and an anti-oxidant N-acetyl-L-cysteine (NAC) significantly repressed LPS-induced PI3K/Akt phosphorylation and the downstream IKK/IkappaB activation. NAC thereby inhibited LPS-induced iNOS expression and NO production. The present results suggest that the anti-inflammatory effect of Ampelopsin is due to inhibiting the interconnected ROS/Akt/IKK/NF-kappaB signaling pathways.

Ampelopsin inhibits H(2)O(2)-induced apoptosis by ERK and Akt signaling pathways and up-regulation of heme oxygenase-1.[Pubmed:22144097]

Phytother Res. 2012 Jul;26(7):988-94.

Oxidative stress plays an important role in neurodegenerative disorders. Ampelopsin, a flavonoid abundant in Rattan tea (Ampelopsis grossedentata), is a potent antioxidant and its neuroprotective effect against H(2)O(2)-induced apoptosis in PC12 cells is investigated here for the first time. It was found that treatment of cells with Ampelopsin for 1 h significantly reduced the loss of vitality, LDH release and apoptosis and inhibited the formation of reactive oxygen species (ROS). Ampelopsin was able to prevent the activation of p38 induced by H(2)O(2). In addition, up-regulation of heme oxygenase-1 (HO-1) expression by Ampelopsin was shown to be both dose- and time-dependent. Mechanically, HO-1 expression induced by Ampelopsin was found to be due to activation of the ERK and Akt signaling pathways, because it was almost completely blocked by the specific inhibitors of ERK and Akt. These results suggest that Ampelopsin increases cellular antioxidant defense through activation of the ERK and Akt signaling pathways, which induces HO-1 expression and thereby protects PC12 cells from H(2)O(2)-induced apoptosis.

[Anti-invasive and anti-metastatic effect of ampelopsin on melanoma].[Pubmed:12703989]

Ai Zheng. 2003 Apr;22(4):363-7.

BACKGROUND & OBJECTIVE: The authors had firstly reported that Ampelopsin possess anticancer effects on several human cancer cell lines in vitro and on transplant mouse B16 melanoma in vivo. In order to further explore its antitumor effect, the authors designed this study to investigate the effect of Ampelopsin on invasion and metastasis of B16 melanoma in vivo and in vitro. METHODS: B16 cells were injected into C57BL/6 mouse via tail lateral vein, and subsequently formed an experimental pulmonary metastasis. Ampelopsin was administered at 3 dosages by intraperitoneal injection daily for 18 days from the day before cell injection. The B16 mouse melanoma cells were treated with Ampelopsin for 3 days. The effect of Ampelopsin on invasion, migration,and adhesion of B16 melanoma cells were evaluated using Transwell chambers attached with polycarbonate filters and reconstituted basement membrane (Matrigel). RESULTS: The number of metastases in the mice that were given Ampelopsin at the dosages of 150, 200, and 250 mg/kg significantly reduced as compared to the control (P< 0.05), and the inhibition rates were 30.97%, 40.58%, and 61.16%, respectively. The ability of the Ampelopsin treated B16 cells to invade the reconstituted basement membrane decreased significantly (P< 0.01), and the inhibition rates were 36.06%, 59.58%, and 79.09% for Ampelopsin at 20, 40, and 80 micromol/L, respectively. Ampelopsin can also inhibit B16 cells migration,and the inhibition rates were 51.59%, 56.51%, and 66.75% for Ampelopsin at 20, 40, and 80 micromol/L, respectively (P< 0.01). The ability of adhesion of the B16 cells with fibronectin, laminin, or Matrigel decreased significantly. CONCLUSION: Ampelopsin has anti-invasive and anti-metastatic effects on B16 melanoma.

Hepatoprotective activity of tocha, the stems and leaves of Ampelopsis grossedentata, and ampelopsin.[Pubmed:15630194]

Biofactors. 2004;21(1-4):175-8.

Hepatoprotective effect of the leaves and stems of Ampelopsis grossedentata together with its main constituent, Ampelopsin, were examined on D-galactosamine induced liver injury in rats. The diet containing 50% ethanolic extract (1%) and Ampelopsin (0.1%) markedly suppressed the increase of LDH, ALT, AST, alpha-tocopherol levels and GSG/GSSH caused by GalN treatment. These results suggested that Ampelopsin from Tocha acted to prevent the oxidative stress in vivo that may have been due to active oxygen species formed by a macrophage by the action of GalN.

Description

Dihydromyricetin is a potent inhibitor with an IC50 of 48 μM on dihydropyrimidinase. Dihydromyricetin can activate autophagy through inhibiting mTOR signaling. Dihydromyricetin suppresses the formation of mTOR complexes (mTORC1/2).

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