Procyanidin B2

CAS# 29106-49-8

Procyanidin B2

Catalog No. BCN6315----Order now to get a substantial discount!

Product Name & Size Price Stock
Procyanidin B2: 5mg $75 In Stock
Procyanidin B2: 10mg Please Inquire In Stock
Procyanidin B2: 20mg Please Inquire Please Inquire
Procyanidin B2: 50mg Please Inquire Please Inquire
Procyanidin B2: 100mg Please Inquire Please Inquire
Procyanidin B2: 200mg Please Inquire Please Inquire
Procyanidin B2: 500mg Please Inquire Please Inquire
Procyanidin B2: 1000mg Please Inquire Please Inquire
Related Products

Quality Control of Procyanidin B2

Number of papers citing our products

Chemical structure

Procyanidin B2

3D structure

Chemical Properties of Procyanidin B2

Cas No. 29106-49-8 SDF Download SDF
PubChem ID 360757 Appearance Beige powder
Formula C30H26O12 M.Wt 578.52
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms Proanthocyanidin B2
Solubility DMSO : ≥ 50 mg/mL (86.43 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 2-(3,4-dihydroxyphenyl)-8-[(4R)-2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-3,4-dihydro-2H-chromen-4-yl]-3,4-dihydro-2H-chromene-3,5,7-triol
SMILES C1C(C(OC2=C1C(=CC(=C2C3C(C(OC4=CC(=CC(=C34)O)O)C5=CC(=C(C=C5)O)O)O)O)O)C6=CC(=C(C=C6)O)O)O
Standard InChIKey XFZJEEAOWLFHDH-DAIQQCIXSA-N
Standard InChI InChI=1S/C30H26O12/c31-13-7-20(37)24-23(8-13)41-29(12-2-4-16(33)19(36)6-12)27(40)26(24)25-21(38)10-17(34)14-9-22(39)28(42-30(14)25)11-1-3-15(32)18(35)5-11/h1-8,10,22,26-29,31-40H,9H2/t22?,26-,27?,28?,29?/m1/s1
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 Procyanidin B2

1 Cinnamomum sp. 2 Crataegus sp. 3 Dryopteris sp. 4 Fragaria sp. 5 Harungana sp. 6 Hypericum sp. 7 Juniperus sp. 8 Malus sp. 9 Theobroma sp. 10 Tilia sp. 11 Vaccinium sp. 12 Vitis sp.

Biological Activity of Procyanidin B2

DescriptionProcyanidin B2 has vascular protective, anti-diabetic nephropathy, anti-cancer, anti-inflammatory, and antioxidant activities. Procyanidin B2 inhibited NLRP3 inflammasome activation via suppression of AP-1 pathway, and up-regulated the expression of GSTP1 via a mechanism that involves ERK and p38 MAPK activation and Nrf2 translocation. It has anti- and pro-oxidant effects on metal-mediated DNA damage by interacting with H2O2 and metal ions.
TargetsCaspase | ROS | AP-1 | IL Receptor | COX | NOS | p65 | NO | NF-kB | Nrf2 | ERK | JNK | p38MAPK
In vitro

Mechanisms of DNA methyltransferase-inhibitor interactions: Procyanidin B2 shows new promise for therapeutic intervention of cancer.[Pubmed: 25839702]

Chem Biol Interact. 2015 May 25;233:122-38.

DNA methyltransferases (DNMTs) is a key epigenetic enzyme for pharmacological manipulation and is employed in cancer reprogramming. During past few years multiple strategies have been implemented to excavate epigenetic compounds targeting DNMTs.
METHODS AND RESULTS:
In light of the emerging concept of chemoinformatics, molecular docking and simulation studies have been employed to accelerate the development of DNMT inhibitors. Among the DNMT inhibitors known till date, epigallocathechin-3-gallate (EGCG) was identified to be effective in reducing DNMT activity. However, the broad spectrum of EGCG to other diseases and variable target enzymes offers some limitations. In view of this, 32 EGCG analogues were screened at S-Adnosyl-L-homocysteine (SAH) binding pocket of DNMTs and Procyanidin B2-3, 3'-di-O-gallate (Procyanidin B2) was obtained as potent inhibitor having medicinally relevant chemical space. Further, in vitro analysis demonstrates the efficiency of Procyanidin B2 in attenuating DNMT activity at IC50 of 6.88±0.647 μM and subsequently enhancing the expression of DNMT target genes, E-cadherin, Maspin and BRCA1.
CONCLUSIONS:
Moreover, the toxic property of Procyanidin B2 towards triple negative breast cancer cells to normal cells offers platform for pre-clinical trial and an insight to the treatment of cancer.

Procyanidin B2 inhibits inflammasome-mediated IL-1β production in lipopolysaccharide-stimulated macrophages.[Pubmed: 25379992]

Mol Nutr Food Res. 2015 Feb;59(2):262-9.

Macrophage stimulation with bacterial LPS triggers inflammasome activation, resulting in pro-inflammatory IL-1β cytokine maturation and secretion. IL-1β underlies the pathologies of many diseases, including type-2 diabetes. Thus, the modulation of the inflammatory response through bioactive food compounds, such as procyanidins, is a powerful tool to promote homeostasis.
METHODS AND RESULTS:
To determine the role of Procyanidin B2 in inflammasome activation, LPS-primed THP-1-macrophages were supplemented with or without Procyanidin B2 . Western blot analysis of COX2 , iNOS, p65, NLRP3 and IL-1β was performed followed by p65 supershift assay, in vivo caspase-1 activation assay and NO, IL-1β and IL-6 determination. Procyanidin B2 mediated inhibition of inflammasome activation includes the inactivation of the NF-κB signalling pathway, the first stage required for the transcription of inflammasome precursors, through the inhibition of p65 nuclear expression and DNA binding, resulting in the transcriptional repression of target genes, such as COX2 , iNOS and production of IL-6 and NO. Furthermore, Procyanidin B2 decreases NLRP3 and pro-IL-1β cytoplasmic pools, limiting components of inflammasome activation and impeding inflammasome assembly and caspase-1 activation, and finally secretion of active IL-1β.
CONCLUSIONS:
This study provides the first evidence that Procyanidin B2 inhibits inflammasome activation and IL-1β secretion during LPS-induced acute inflammation in human macrophages.

Procyanidin B2 has anti- and pro-oxidant effects on metal-mediated DNA damage.[Pubmed: 16198231 ]

Free Radic Biol Med. 2005 Oct 15;39(8):1041-9.

Procyanidin B2 (epicatechin-(4beta-8)-epicatechin), which is present in grape seeds, apples, and cacao beans, has antioxidant properties. We investigated the mechanism of preventive action of Procyanidin B2 against oxidative DNA damage in human cultured cells and isolated DNA.
METHODS AND RESULTS:
Procyanidin B2 inhibited the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in the human leukemia cell line HL-60 treated with an H2O2-generating system. In contrast, a high concentration of Procyanidin B2 increased the formation of 8-oxodG in HL-60 cells. Experiments with calf thymus DNA also revealed that Procyanidin B2 decreased 8-oxodG formation by Fe(II)/H2O2, whereas Procyanidin B2 induced DNA damage in the presence of Cu(II), and H2O2 extensively enhanced it. An electron spin resonance spin trapping study utilizing 3,3,5,5-tetramethyl-1-pyrroline-N-oxide (M4PO) demonstrated that Procyanidin B2 decreased the signal of M4PO-OH from H2O2 and Fe(II), whereas Procyanidin B2 enhanced the signal from H2O2 and Cu(II). As an antioxidant mechanism, UV-visible spectroscopy showed that Procyanidin B2 chelated Fe(II) at equivalent concentrations. As a pro-oxidant property, we examined DNA damage induced by Procyanidin B2, using 32P-labeled DNA fragments obtained from genes relevant to human cancer.
CONCLUSIONS:
Our results raise the possibility that Procyanidin B2 exerts both antioxidant and pro-oxidant properties by interacting with H2O2 and metal ions.

In vivo

Effect of cinnamon and its procyanidin-B2 enriched fraction on diabetic nephropathy in rats.[Pubmed: 25199697]

Chem Biol Interact. 2014 Sep 6;222C:68-76.

Non-enzymatic protein glycation and resultant accumulation of advanced glycation endproducts (AGE) are implicated in the pathogenesis of diabetic complications including diabetic nephropathy (DN). It is considered that antiglycating agents offer protection against AGE mediated pathologies including DN. Earlier we characterized procyanidin-B2 (PCB2) as the active component from cinnamon (Cinnamomum zeylanicum) that inhibits AGE formation in vitro.
METHODS AND RESULTS:
In this study, we have investigated the potential of PCB2-enriched fraction of cinnamon to prevent in vivo accumulation of AGE and to ameliorate renal changes in diabetic rats. Streptozotocin-induced diabetic rats were fed with either 3% cinnamon or 0.002% PCB2-fraction in diet for 12weeks. Biochemical analysis of blood and urine was performed at the end of experiment. Evaluation of glomerular markers that serve as indicators of renal function was done by immunohistochemistry, immunoblotting and qRT-PCR. Supplementation of diabetic rats with cinnamon and PCB2-fraction prevented glycation mediated RBC-IgG cross-links and HbA1c accumulation in diabetes rats. Cinnamon and PCB2-fraction also inhibited the accumulation of N-carboxy methyl lysine (CML), a prominent AGE in diabetic kidney. Interestingly, cinnamon and its PCB2-fraction prevented the AGE mediated loss of expression of glomerular podocyte proteins; nephrin and podocin. Inhibition of AGE by cinnamon and PCB2-fraction ameliorated the diabetes mediated renal malfunction in rats as evidenced by reduced urinary albumin and creatinine.
CONCLUSIONS:
In conclusion, PCB2 from cinnamon inhibited AGE accumulation in diabetic rat kidney and ameliorated AGE mediated pathogenesis of DN.

Protocol of Procyanidin B2

Cell Research

Procyanidin B2 induces Nrf2 translocation and glutathione S-transferase P1 expression via ERKs and p38-MAPK pathways and protect human colonic cells against oxidative stress.[Pubmed: 22042007 ]

Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells.[Pubmed: 25450671]

Biochem Pharmacol. 2014 Dec 15;92(4):599-606.

Procyanidins are the flavanols from polyphenols commonly found in fruits and red wine. Recent studies have shown that procyanidins possess potential anti-inflammatory activities. However, underlying mechanisms remain to be understood. Inflammasomes are multi-protein complexes composed of pro-caspase and pattern recognition receptors (PRRs) such as NOD-like receptor family, pyrin domain containing 3 (NLRP3).
METHODS AND RESULTS:
Since aberrant activation of NLRP3 inflammasome is implicated in the pathogeneses of pro-inflammatory diseases such as diabetes, atherosclerosis and arthritis, we aimed to investigate whether Procyanidin B2 (PCB2), the most widely distributed natural procyanidins, inhibits the activation of NLRP3 inflammasome in endothelial cells (ECs). We found that, in human umbilical vein ECs (HUVECs), PCB2 significantly suppressed the activation of NLRP3 inflammasome and inhibited subsequent caspase-1 activation and interleukin (IL)-1β secretion in response to lipopolysaccharides (LPS). PCB2 negatively regulated the gene expression of NLRP3. In addition, PCB2 attenuated LPS-induced production of reactive oxygen species (ROS) and the transcriptional activity of activator protein-1 (AP-1). In conclusion, we demonstrated for the first time that Procyanidin B2 inhibits NLRP3 inflammasome activation via suppression of AP-1 pathway in ECs.
CONCLUSIONS:
These results suggest a new mechanism by which natural flavoids such as procyanidins exert their vascular protective effects.

Eur J Nutr. 2012 Oct;51(7):881-92.

Procyanidin B2 (PB2) is a naturally occurring flavonoid widely found in cocoa, red wine and grape juice. Recent studies have suggested that PB2 could protect against oxidative stress- and chemical-induced injury in colonic cells by modulating the endogenous cellular defence. However, the precise mechanism for this protection is not fully understood. Herein, we examined the effect of PB2 on the expression of one of the major antioxidant/detoxificant enzymes related to intestinal protection, the glutathione S-transferase P1 (GSTP1), and the molecular mechanisms involved.
METHODS AND RESULTS:
Human colonic Caco-2 cells were treated with PB2 at different times and enzymatic activity, and mRNA and protein levels of GSTP1 were evaluated. The nuclear translocation of the transcription factor NF-erythroid 2-related factor (Nrf2) and the phosphorylation states of specific proteins central to intracellular signalling cascades were also investigated. PB2 induced the expression and activity of GSTP1 and the nuclear translocation of Nrf2. Interestingly, two important signalling proteins involved in Nrf2 translocation, the extracellular signal-regulated protein kinases (ERKs) and the p38 mitogen-activated protein kinase (MAPK) were also activated. Further experiments with specific inhibitors of both pathways confirmed their critical role in the beneficial effects induced by PB2.
CONCLUSIONS:
The present results show that PB2 protects against oxidative injury in colonic cells and up-regulate the expression of GSTP1 via a mechanism that involves ERK and p38 MAPK activation and Nrf2 translocation. These results provide a molecular basis for the potential contribution of PB2 in the prevention of oxidative stress-related intestinal injury and gut pathologies.

Procyanidin B2 Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Procyanidin B2 Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Procyanidin B2

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.7285 mL 8.6427 mL 17.2855 mL 34.571 mL 43.2137 mL
5 mM 0.3457 mL 1.7285 mL 3.4571 mL 6.9142 mL 8.6427 mL
10 mM 0.1729 mL 0.8643 mL 1.7285 mL 3.4571 mL 4.3214 mL
50 mM 0.0346 mL 0.1729 mL 0.3457 mL 0.6914 mL 0.8643 mL
100 mM 0.0173 mL 0.0864 mL 0.1729 mL 0.3457 mL 0.4321 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Procyanidin B2

Procyanidin B2 is a natural flavonoid, with anti-cancer, antioxidant activities.

In Vitro:Procyanidin B2 shows antiproliferative activity to MCF-7 cells, with an IC50 of 19.21 μM. However, Procyanidin B2 exhibits no effect on DNA-ladder formation[1]. Procyanidin B2 (0.1, 1, 2 μM) inhibits the activation of pyrin domain containing 3 (NLRP3) inflammasome in human umbilical vein ECs (HUVECs), and the inhibition is via suppression of AP-1 activity, and such effect can be abolished by overexpression of c-Jun. Procyanidin B2 (2 μM for 12 h) also reduces ROS in HUVECs[2].

In Vivo:Procyanidin B2 (40, 20, and 10 mg/kg, p.o.) protects against cerebral ischemia-induced infarct volume and brain edema in rats. Procyanidin B2 (40 mg/kg, p.o) also improves functional outcomes, regulates blood-brain barrier (BBB) permeability after cerebral ischemia. Moreover, Procyanidin B2 attenuates cerebral ischemia-induced tight junction degradation, mitochondrial depolarization and intracellular oxidative stress. Procyanidin B2 (40 mg/kg, p.o) increases Nrf2 activation and HO-1, GSTα, and NQO1 protein expression in normal brains in vivo[3].

References:
[1]. Avelar MM, et al. Procyanidin b2 cytotoxicity to mcf-7 human breast adenocarcinoma cells. Indian J Pharm Sci. 2012 Jul;74(4):351-5. [2]. Yang H, et al. Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells. Biochem Pharmacol. 2014 Dec 15;92(4):599-606. [3]. Wu S, et al. Procyanidin B2 attenuates neurological deficits and blood-brain barrier disruption in a rat model of cerebral ischemia. Mol Nutr Food Res. 2015 Oct;59(10):1930-41.

Featured Products
New Products
 

References on Procyanidin B2

Procyanidin B2 inhibits inflammasome-mediated IL-1beta production in lipopolysaccharide-stimulated macrophages.[Pubmed:25379992]

Mol Nutr Food Res. 2015 Feb;59(2):262-9.

SCOPE: Macrophage stimulation with bacterial LPS triggers inflammasome activation, resulting in pro-inflammatory IL-1beta cytokine maturation and secretion. IL-1beta underlies the pathologies of many diseases, including type-2 diabetes. Thus, the modulation of the inflammatory response through bioactive food compounds, such as procyanidins, is a powerful tool to promote homeostasis. METHODS AND RESULTS: To determine the role of Procyanidin B2 in inflammasome activation, LPS-primed THP-1-macrophages were supplemented with or without Procyanidin B2 . Western blot analysis of COX2 , iNOS, p65, NLRP3 and IL-1beta was performed followed by p65 supershift assay, in vivo caspase-1 activation assay and NO, IL-1beta and IL-6 determination. Procyanidin B2 mediated inhibition of inflammasome activation includes the inactivation of the NF-kappaB signalling pathway, the first stage required for the transcription of inflammasome precursors, through the inhibition of p65 nuclear expression and DNA binding, resulting in the transcriptional repression of target genes, such as COX2 , iNOS and production of IL-6 and NO. Furthermore, Procyanidin B2 decreases NLRP3 and pro-IL-1beta cytoplasmic pools, limiting components of inflammasome activation and impeding inflammasome assembly and caspase-1 activation, and finally secretion of active IL-1beta. CONCLUSION: This study provides the first evidence that Procyanidin B2 inhibits inflammasome activation and IL-1beta secretion during LPS-induced acute inflammation in human macrophages.

Procyanidin B2 induces Nrf2 translocation and glutathione S-transferase P1 expression via ERKs and p38-MAPK pathways and protect human colonic cells against oxidative stress.[Pubmed:22042007]

Eur J Nutr. 2012 Oct;51(7):881-92.

PURPOSE: Procyanidin B2 (PB2) is a naturally occurring flavonoid widely found in cocoa, red wine and grape juice. Recent studies have suggested that PB2 could protect against oxidative stress- and chemical-induced injury in colonic cells by modulating the endogenous cellular defence. However, the precise mechanism for this protection is not fully understood. Herein, we examined the effect of PB2 on the expression of one of the major antioxidant/detoxificant enzymes related to intestinal protection, the glutathione S-transferase P1 (GSTP1), and the molecular mechanisms involved. METHODS: Human colonic Caco-2 cells were treated with PB2 at different times and enzymatic activity, and mRNA and protein levels of GSTP1 were evaluated. The nuclear translocation of the transcription factor NF-erythroid 2-related factor (Nrf2) and the phosphorylation states of specific proteins central to intracellular signalling cascades were also investigated. RESULTS: PB2 induced the expression and activity of GSTP1 and the nuclear translocation of Nrf2. Interestingly, two important signalling proteins involved in Nrf2 translocation, the extracellular signal-regulated protein kinases (ERKs) and the p38 mitogen-activated protein kinase (MAPK) were also activated. Further experiments with specific inhibitors of both pathways confirmed their critical role in the beneficial effects induced by PB2. CONCLUSIONS: The present results show that PB2 protects against oxidative injury in colonic cells and up-regulate the expression of GSTP1 via a mechanism that involves ERK and p38 MAPK activation and Nrf2 translocation. These results provide a molecular basis for the potential contribution of PB2 in the prevention of oxidative stress-related intestinal injury and gut pathologies.

Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells.[Pubmed:25450671]

Biochem Pharmacol. 2014 Dec 15;92(4):599-606.

Procyanidins are the flavanols from polyphenols commonly found in fruits and red wine. Recent studies have shown that procyanidins possess potential anti-inflammatory activities. However, underlying mechanisms remain to be understood. Inflammasomes are multi-protein complexes composed of pro-caspase and pattern recognition receptors (PRRs) such as NOD-like receptor family, pyrin domain containing 3 (NLRP3). Since aberrant activation of NLRP3 inflammasome is implicated in the pathogeneses of pro-inflammatory diseases such as diabetes, atherosclerosis and arthritis, we aimed to investigate whether Procyanidin B2 (PCB2), the most widely distributed natural procyanidins, inhibits the activation of NLRP3 inflammasome in endothelial cells (ECs). We found that, in human umbilical vein ECs (HUVECs), PCB2 significantly suppressed the activation of NLRP3 inflammasome and inhibited subsequent caspase-1 activation and interleukin (IL)-1beta secretion in response to lipopolysaccharides (LPS). PCB2 negatively regulated the gene expression of NLRP3. In addition, PCB2 attenuated LPS-induced production of reactive oxygen species (ROS) and the transcriptional activity of activator protein-1 (AP-1). In conclusion, we demonstrated for the first time that Procyanidin B2 inhibits NLRP3 inflammasome activation via suppression of AP-1 pathway in ECs. These results suggest a new mechanism by which natural flavoids such as procyanidins exert their vascular protective effects.

Mechanisms of DNA methyltransferase-inhibitor interactions: Procyanidin B2 shows new promise for therapeutic intervention of cancer.[Pubmed:25839702]

Chem Biol Interact. 2015 May 25;233:122-38.

DNA methyltransferases (DNMTs) is a key epigenetic enzyme for pharmacological manipulation and is employed in cancer reprogramming. During past few years multiple strategies have been implemented to excavate epigenetic compounds targeting DNMTs. In light of the emerging concept of chemoinformatics, molecular docking and simulation studies have been employed to accelerate the development of DNMT inhibitors. Among the DNMT inhibitors known till date, epigallocathechin-3-gallate (EGCG) was identified to be effective in reducing DNMT activity. However, the broad spectrum of EGCG to other diseases and variable target enzymes offers some limitations. In view of this, 32 EGCG analogues were screened at S-Adnosyl-L-homocysteine (SAH) binding pocket of DNMTs and Procyanidin B2-3, 3'-di-O-gallate (Procyanidin B2) was obtained as potent inhibitor having medicinally relevant chemical space. Further, in vitro analysis demonstrates the efficiency of Procyanidin B2 in attenuating DNMT activity at IC50 of 6.88+/-0.647 muM and subsequently enhancing the expression of DNMT target genes, E-cadherin, Maspin and BRCA1. Moreover, the toxic property of Procyanidin B2 towards triple negative breast cancer cells to normal cells offers platform for pre-clinical trial and an insight to the treatment of cancer.

Procyanidin B2 has anti- and pro-oxidant effects on metal-mediated DNA damage.[Pubmed:16198231]

Free Radic Biol Med. 2005 Oct 15;39(8):1041-9.

Procyanidin B2 (epicatechin-(4beta-8)-epicatechin), which is present in grape seeds, apples, and cacao beans, has antioxidant properties. We investigated the mechanism of preventive action of Procyanidin B2 against oxidative DNA damage in human cultured cells and isolated DNA. Procyanidin B2 inhibited the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in the human leukemia cell line HL-60 treated with an H2O2-generating system. In contrast, a high concentration of Procyanidin B2 increased the formation of 8-oxodG in HL-60 cells. Experiments with calf thymus DNA also revealed that Procyanidin B2 decreased 8-oxodG formation by Fe(II)/H2O2, whereas Procyanidin B2 induced DNA damage in the presence of Cu(II), and H2O2 extensively enhanced it. An electron spin resonance spin trapping study utilizing 3,3,5,5-tetramethyl-1-pyrroline-N-oxide (M4PO) demonstrated that Procyanidin B2 decreased the signal of M4PO-OH from H2O2 and Fe(II), whereas Procyanidin B2 enhanced the signal from H2O2 and Cu(II). As an antioxidant mechanism, UV-visible spectroscopy showed that Procyanidin B2 chelated Fe(II) at equivalent concentrations. As a pro-oxidant property, we examined DNA damage induced by Procyanidin B2, using 32P-labeled DNA fragments obtained from genes relevant to human cancer. Our results raise the possibility that Procyanidin B2 exerts both antioxidant and pro-oxidant properties by interacting with H2O2 and metal ions.

Procyanidin B2 and a cocoa polyphenolic extract inhibit acrylamide-induced apoptosis in human Caco-2 cells by preventing oxidative stress and activation of JNK pathway.[Pubmed:21334869]

J Nutr Biochem. 2011 Dec;22(12):1186-94.

Humans are exposed to dietary acrylamide (AA) during their lifetime; it is therefore necessary to investigate the mechanisms associated with AA induced toxic effects. Accumulating evidence indicates that oxidative stress may contribute to AA cytotoxicity, but the link between oxidative stress and AA cytotoxicity in the gastrointestinal tract, the primary organ in contact with dietary AA, has not been described. In this study, we evaluate the alterations of the redox balance induced by AA in Caco-2 intestinal cells as well as the potential protective role of natural antioxidants such as a well-standardized cocoa polyphenolic extract (CPE) and its main polyphenol components epicatechin (EC) and Procyanidin B2 (PB2). We found that AA-induced oxidative stress in Caco-2 cells is evidenced by glutathione (GSH) depletion and reactive oxygen species (ROS) overproduction. AA also activated the extracellular-regulated kinases and the c-Jun N-amino terminal kinases (JNKs) leading to an increase in caspase-3 activity and cell death. Studies with appropriate inhibitors confirmed the implication of oxidative stress and JNKs activation in AA-induced apoptosis. Additionally, AA cytotoxicity was counteracted by CPE or PB2 by inhibiting GSH consumption and ROS generation, increasing the levels of gamma-glutamyl cysteine synthase and glutathione-S-transferase and blocking the apoptotic pathways activated by AA. Therefore, AA-induced cytotoxicity and apoptosis are closely related to oxidative stress in Caco-2 cells. Interestingly, natural dietary antioxidant such as PB2 and CPE were able to suppress AA toxicity by improving the redox status of Caco-2 cells and by blocking the apoptotic pathway activated by AA.

Effect of cinnamon and its procyanidin-B2 enriched fraction on diabetic nephropathy in rats.[Pubmed:25199697]

Chem Biol Interact. 2014 Oct 5;222:68-76.

Non-enzymatic protein glycation and resultant accumulation of advanced glycation endproducts (AGE) are implicated in the pathogenesis of diabetic complications including diabetic nephropathy (DN). It is considered that antiglycating agents offer protection against AGE mediated pathologies including DN. Earlier we characterized procyanidin-B2 (PCB2) as the active component from cinnamon (Cinnamomum zeylanicum) that inhibits AGE formation in vitro. In this study, we have investigated the potential of PCB2-enriched fraction of cinnamon to prevent in vivo accumulation of AGE and to ameliorate renal changes in diabetic rats. Streptozotocin-induced diabetic rats were fed with either 3% cinnamon or 0.002% PCB2-fraction in diet for 12weeks. Biochemical analysis of blood and urine was performed at the end of experiment. Evaluation of glomerular markers that serve as indicators of renal function was done by immunohistochemistry, immunoblotting and qRT-PCR. Supplementation of diabetic rats with cinnamon and PCB2-fraction prevented glycation mediated RBC-IgG cross-links and HbA1c accumulation in diabetes rats. Cinnamon and PCB2-fraction also inhibited the accumulation of N-carboxy methyl lysine (CML), a prominent AGE in diabetic kidney. Interestingly, cinnamon and its PCB2-fraction prevented the AGE mediated loss of expression of glomerular podocyte proteins; nephrin and podocin. Inhibition of AGE by cinnamon and PCB2-fraction ameliorated the diabetes mediated renal malfunction in rats as evidenced by reduced urinary albumin and creatinine. In conclusion, PCB2 from cinnamon inhibited AGE accumulation in diabetic rat kidney and ameliorated AGE mediated pathogenesis of DN.

Description

Procyanidin B2 is a natural flavonoid, with anti-cancer, antioxidant activities.

Keywords:

Procyanidin B2,29106-49-8,Proanthocyanidin B2,Natural Products, buy Procyanidin B2 , Procyanidin B2 supplier , purchase Procyanidin B2 , Procyanidin B2 cost , Procyanidin B2 manufacturer , order Procyanidin B2 , high purity Procyanidin B2

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: