Brazilin

CAS# 474-07-7

Brazilin

Catalog No. BCN5529----Order now to get a substantial discount!

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Quality Control of Brazilin

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Chemical structure

Brazilin

3D structure

Chemical Properties of Brazilin

Cas No. 474-07-7 SDF Download SDF
PubChem ID 73384 Appearance Yellowish powder
Formula C16H14O5 M.Wt 286.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Solubility Soluble in methan
Chemical Name (6aS,11bR)-7,11b-dihydro-6H-indeno[2,1-c]chromene-3,6a,9,10-tetrol
SMILES C1C2=CC(=C(C=C2C3C1(COC4=C3C=CC(=C4)O)O)O)O
Standard InChIKey UWHUTZOCTZJUKC-JKSUJKDBSA-N
Standard InChI InChI=1S/C16H14O5/c17-9-1-2-10-14(4-9)21-7-16(20)6-8-3-12(18)13(19)5-11(8)15(10)16/h1-5,15,17-20H,6-7H2/t15-,16+/m0/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 Brazilin

The heartwoods of Caesalpinia sappan L.

Biological Activity of Brazilin

DescriptionBrazilin exhibits cancer preventive, anti-hepatotoxicity, antiplatelet activity, and anti-inflammatory activities, it also inhibits UVB-induced MMP-1/3 expressions and secretions by suppressing of NF-κB activation in human dermal fibroblasts, thus, it might be used as a potential agent for treatment of UV-induced skin photoaging. Brazilin has anti-IKK activity, can selectively disrupt proximal IL-1 receptor signaling complex formation by targeting an IKK-upstream signaling components. Brazilin induces vasorelaxation by the increasing intracellular Ca(2+) concentration in endothelial cells of blood vessels and hence activating Ca(2+)/calmodulin-dependent NO synthesis.
TargetsIL Receptor | TLR | TNF-α | PI3K | Akt | ERK | p38MAPK | MMP(e.g.TIMP) | NOS | NO | Calcium Channel | NF-kB | IkB | HO-1 | IKK
In vitro

Brazilin inhibits UVB-induced MMP-1/3 expressions and secretions by suppressing the NF-κB pathway in human dermal fibroblasts.[Pubmed: 22044921 ]

Eur J Pharmacol. 2012 Jan 15;674(2-3):80-6.

Brazilin (7, 11b-dihydrobenz[b]indeno[1,2-d]pyran-3,6a,9,10 (6H)-tetrol), the major component of Caesalpinia sappan L., is a natural red pigment used for histological staining.
METHODS AND RESULTS:
Recent studies have shown that Brazilin exhibits distinct biological effects, including anti-hepatotoxicity, antiplatelet activity, and anti-inflammatory activities. In the present study, we evaluated the effects of Brazilin on MMP-1 and -3 expressions in human dermal fibroblasts exposed to ultraviolet B (UVB) irradiation. Brazilin showed protective effect on UVB-induced loss of cell viability of fibroblasts. Brazilin also blocked significantly UVB-induced Reactive Oxygen Species generation in fibroblasts. Brazilin inhibited UVB-induced MMP-1/3 expressions and secretions in a dose-dependent manner. Moreover, UVB-induced NF-κB activation was completely blocked by treatment with Brazilin.
CONCLUSIONS:
These findings suggest that Brazilin inhibits UVB-induced MMP-1/3 expressions and secretions by suppressing of NF-κB activation in human dermal fibroblasts. Thus, Brazilin might be used as a potential agent for treatment of UV-induced skin photoaging.

Induction of vasorelaxation through activation of nitric oxide synthase in endothelial cells by brazilin.[Pubmed: 12729841]

Eur J Pharmacol. 2003 May 2;468(1):37-45.

The vasorelaxant activity of Caesalpinia sappan L., a traditional Chinese medicine, and its major component Brazilin were investigated in isolated rat aorta and human umbilical vein endothelial cells.
METHODS AND RESULTS:
In isolated rat aorta, C. sappan L. extract and Brazilin relaxed phenylephrine-induced vasocontraction and increased cyclic guanosine 3',5'-monophosphate (cGMP) content. Induction of vasorelaxation of Brazilin was endothelium-dependent and could be markedly blocked by pretreatment with nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME); N(G)-monomethyl-L-arginine acetate (L-NMMA) and guanylyl cyclase inhibitor, methylene blue; 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and nitric oxide (NO) scavenger, hemoglobin. The increasing cGMP content induced by Brazilin was also blocked by pretreatment with L-NAME, methylene blue, and the removal of extracellular Ca(2+). In human umbilical vein endothelial cells, Brazilin dose-dependently induced an increase in NO formation and NOS activity, which were greatly attenuated by either the removal of extracellular Ca(2+) or the chelating of intracellular Ca(2+) chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). Moreover, Brazilin dose-dependently induced the influx of extracellular Ca(2+) in human umbilical vein endothelial cells.
CONCLUSIONS:
Collectively, these results suggest that Brazilin induces vasorelaxation by the increasing intracellular Ca(2+) concentration in endothelial cells of blood vessels and hence activating Ca(2+)/calmodulin-dependent NO synthesis. The NO is released and then transferred into smooth muscle cells to activate guanylyl cyclase and increase cGMP content, resulting in vasorelaxation.

In vivo

Brazilin plays an anti-inflammatory role with regulating Toll-like receptor 2 and TLR 2 downstream pathways in Staphylococcus aureus-induced mastitis in mice.[Pubmed: 25939535]

Int Immunopharmacol. 2015 Jul;27(1):130-7.

Mastitis, which commonly occurs during the postpartum period, is caused by the infection of the mammary glands. The most common infectious bacterial pathogen of mastitis is Staphylococcus aureus (S. aureus) in both human and animals. Brazilin, a compound isolated from the traditional herbal medicine Caesalpinia sappan L., has been shown to exhibit multiple biological properties.
METHODS AND RESULTS:
The present study was performed to determine the effect of Brazilin on the inflammatory response in the mouse model of S. aureus mastitis and to confirm the mechanism of action involved. Brazilin treatment was applied in both a mouse model and cells. After Brazilin treatment of cells, Western blotting and qPCR were performed to detect the protein levels and mRNA levels, respectively. Brazilin treatment significantly attenuated inflammatory cell infiltration and inhibited the expressions of TNF-α, IL-1β and IL-6 in a dose-dependent manner. Administration of Brazilin in mice suppressed S. aureus-induced inflammatory injury and the production of proinflammatory mediators. This suppression was achieved by reducing the increased expression of TLR2 and regulating the NF-κB and MAPK signaling pathways in the mammary gland tissues and cells with S. aureus-induced mastitis.
CONCLUSIONS:
These results suggest that Brazilin appears to be an effective drug for the treatment of mastitis and may be applied as a clinical therapy.

Protocol of Brazilin

Kinase Assay

Upregulation of heme oxygenase-1 by brazilin via the phosphatidylinositol 3-kinase/Akt and ERK pathways and its protective effect against oxidative injury.[Pubmed: 18021765 ]

Brazilin selectively disrupts proximal IL-1 receptor signaling complex formation by targeting an IKK-upstream signaling components.[Pubmed: 24735611]

Biochem Pharmacol. 2014 Jun 15;89(4):515-25.

The ligation of interleukin-1 receptor (IL-1R) or tumor necrosis factor receptor 1 (TNFR1) induces the recruitment of adaptor proteins and their concomitant ubiquitination to the proximal receptor signaling complex, respectively. Such are upstream signaling events of IKK that play essential roles in NF-κB activation. Thus, the discovery of a substance that would modulate the recruitment of key proximal signaling elements at the upstream level of IKK has been impending in this field of study.
METHODS AND RESULTS:
Here, we propose that Brazilin, an active compound of Caesalpinia sappan L. (Leguminosae), is a potent NF-κB inhibitor that selectively disrupts the formation of the upstream IL-1R signaling complex. Analysis of upstream signaling events revealed that Brazilin markedly abolished the IL-1β-induced polyubiquitination of IRAK1 and its interaction with IKK-γ counterpart. Notably, pretreatment of Brazilin drastically interfered the recruitment of the receptor-proximal signaling components including IRAK1/4 and TRAF6 onto MyD88 in IL-1R-triggerd NF-κB activation. Interestingly, Brazilin did not affect the TNF-induced RIP1 ubiquitination and the recruitment of RIP1 and TRAF2 to TNFR1, suggesting that Brazilin is effective in selectively suppressing the proximal signaling complex formation of IL-1R, but not that of TNFR1. Moreover, our findings suggest that such a disruption of IL-1R-proximal complex formation by Brazilin is not mediated by affecting the heterodimerization of IL-1R and IL-1RAcP.
CONCLUSIONS:
Taken together, the results suggest that the anti-IKK activity of Brazilin is induced by targeting IKK upstream signaling components and subsequently disrupting proximal IL-1 receptor signaling complex formation.

Eur J Pharmacol. 2008 Feb 2;580(1-2):12-8.

Heme oxygenase (HO)-1 is a cytoprotective enzyme that is activated by various phytochemicals. We examined the ability of Brazilin to upregulate HO-1 expression in auditory cells.
METHODS AND RESULTS:
We found that Brazilin induced the expressions of HO-1 mRNA and protein in concentration- and time-dependent manners. Brazilin induced nuclear factor-E2-related factor 2 (Nrf2) nuclear translocation, and dominant-negative Nrf2 attenuated Brazilin-induced expression of HO-1. Brazilin induced a temporary increase in the phosphorylation of Akt. While LY294002, a non-selective phosphotidylinositol 3-kinase (PI3K) inhibitor, was able to reduce Brazilin-induced phosphorylation of Akt and the subsequent induction of HO-1. Brazilin activated the extracellular signal-regulated kinase (ERK) and p38 pathways, and the ERK pathway played an important role in HO-1 expression. Brazilin protected the cells against t-butyl hydroperoxide (t-BHP)-induced cell death. The protective effect of Brazilin was abrogated by anti-sense oligodeoxynucleotides (ODN) against the HO-1 gene.
CONCLUSIONS:
These results demonstrate that the expression of HO-1 by Brazilin is mediated via the PI3K/Akt and ERK pathways, and this expression inhibits t-BHP-induced cell death in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells.

Cell Research

c-Fos is involved in inhibition of human bladder carcinoma T24 cells by Brazilin.[Pubmed: 25865820]

IUBMB Life. 2015 Mar;67(3):175-81.

Crude Brazilin extract from Sappan wood has demonstrated strong anti tumor activity in the mouse model of human bladder carcinoma and clinical trial for intravesical therapy. Purified Brazilin was confirmed the most active molecule in inhibition of bladder carcinoma T24 cells.
METHODS AND RESULTS:
Brazilin decreased proliferation and viability of T24 cells in a dose- and time-dependent manner, with a calculated LC50 of 32 μg/mL. More than 1,000 of genes were found upregulated and down regulated by Brazilin treatment in digital gene expression profiling. Gene ontology analysis indicated that stress response, apoptosis, and cell cycle regulatory pathways were highly enriched. Among the regulated genes, c-Fos was the most and specifically upregulated. Overexpression of c-Fos in T24 cells resulted in tumor cell specific changes in cell morphology and viability. Over expression of stress-responsive gene, HSP70, and other highly upregulated genes did not have any effect on cell growth.
CONCLUSIONS:
Brazilin may inhibit T24 cell growth and trigger cell death through a c-Fos-mediated and tumor cell specific signaling pathway. Further studies of its down stream mediators may help to identify better tumor cell type specific drug targets.

Animal Research

Brazilin isolated from Caesalpinia sappan L. inhibits rheumatoid arthritis activity in a type-II collagen induced arthritis mouse model.[Pubmed: 25896410]

BMC Complement Altern Med. 2015 Apr 22;15(1):124.

Caesalpinia sappan L. extracts exhibit great therapeutic potential, and have been shown to have analgesic and anti-inflammatory properties. This study aimed to understand the anti-rheumatoid activity of Brazilin that was isolated from ethyl acetate extract of C. sappan L. The evaluations were conducted in mice with type-II collagen-induced arthritis (CIA).
METHODS AND RESULTS:
Brazilin was purified via preparative HPLC and identified by mass spectrometry and 1H/13C NMR analysis. DBA/1J mice were divided into four groups (n=10). Three groups of mice received intradermal injections of inducer bovine type-II collagen (BTIIC; 2 mg/ml in 0.05 ml acetic acid) and 0.1 ml of booster complete Freund's adjuvant (CFA). A second injection of BTIIC with booster incomplete Freund's adjuvant (ICFA) was given subsequently after 21 days. On 22nd day, purified Brazilin (10 mg/kg body weight) or the disease-modifying anti-rheumatic drug methotrexate (3 mg/kg body weight) was administered intraperitoneally daily or every three days for 21 days, respectively to two groups of mice. At the 42nd day, mice sera were collected, and the levels of pro-inflammatory cytokines and stress enzyme markers in serum were measured using standard immunoassay methods. The microstructure and morphometric analyses of the bones were assessed using high-resolution microfocal computed tomography. Brazilin isolated from C. sappan reduced the arthritis index score and the extent of acute inflammatory paw edema in CIA-mice. The bone mineral density was significantly (p<0.05) lower in only-CIA mice, and appeared to increase commensurate with methotrexate and Brazilin administration. Brazilin prevented joint destruction, surface erosion, and enhanced bone formation as revealed by microstructural examinations. Brazilin markedly attenuated mouse CIA and reduced the serum levels of inflammatory cytokines including TNF-α, IL-1β, and IL-6.
CONCLUSIONS:
Brazilin purified from C. sappan L. shows protective efficacy in CIA mouse, and may be useful to treat chronic inflammatory disorders including rheumatoid arthritis.

Brazilin Dilution Calculator

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Preparing Stock Solutions of Brazilin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.4928 mL 17.4642 mL 34.9284 mL 69.8568 mL 87.321 mL
5 mM 0.6986 mL 3.4928 mL 6.9857 mL 13.9714 mL 17.4642 mL
10 mM 0.3493 mL 1.7464 mL 3.4928 mL 6.9857 mL 8.7321 mL
50 mM 0.0699 mL 0.3493 mL 0.6986 mL 1.3971 mL 1.7464 mL
100 mM 0.0349 mL 0.1746 mL 0.3493 mL 0.6986 mL 0.8732 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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References on Brazilin

Upregulation of heme oxygenase-1 by brazilin via the phosphatidylinositol 3-kinase/Akt and ERK pathways and its protective effect against oxidative injury.[Pubmed:18021765]

Eur J Pharmacol. 2008 Feb 2;580(1-2):12-8.

Heme oxygenase (HO)-1 is a cytoprotective enzyme that is activated by various phytochemicals. We examined the ability of Brazilin to upregulate HO-1 expression in auditory cells. We found that Brazilin induced the expressions of HO-1 mRNA and protein in concentration- and time-dependent manners. Brazilin induced nuclear factor-E2-related factor 2 (Nrf2) nuclear translocation, and dominant-negative Nrf2 attenuated Brazilin-induced expression of HO-1. Brazilin induced a temporary increase in the phosphorylation of Akt. While LY294002, a non-selective phosphotidylinositol 3-kinase (PI3K) inhibitor, was able to reduce Brazilin-induced phosphorylation of Akt and the subsequent induction of HO-1. Brazilin activated the extracellular signal-regulated kinase (ERK) and p38 pathways, and the ERK pathway played an important role in HO-1 expression. Brazilin protected the cells against t-butyl hydroperoxide (t-BHP)-induced cell death. The protective effect of Brazilin was abrogated by anti-sense oligodeoxynucleotides (ODN) against the HO-1 gene. These results demonstrate that the expression of HO-1 by Brazilin is mediated via the PI3K/Akt and ERK pathways, and this expression inhibits t-BHP-induced cell death in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells.

c-Fos is involved in inhibition of human bladder carcinoma T24 cells by brazilin.[Pubmed:25865820]

IUBMB Life. 2015 Mar;67(3):175-81.

Crude Brazilin extract from Sappan wood has demonstrated strong anti tumor activity in the mouse model of human bladder carcinoma and clinical trial for intravesical therapy. Purified Brazilin was confirmed the most active molecule in inhibition of bladder carcinoma T24 cells. Brazilin decreased proliferation and viability of T24 cells in a dose- and time-dependent manner, with a calculated LC50 of 32 microg/mL. More than 1,000 of genes were found upregulated and down regulated by Brazilin treatment in digital gene expression profiling. Gene ontology analysis indicated that stress response, apoptosis, and cell cycle regulatory pathways were highly enriched. Among the regulated genes, c-Fos was the most and specifically upregulated. Overexpression of c-Fos in T24 cells resulted in tumor cell specific changes in cell morphology and viability. Over expression of stress-responsive gene, HSP70, and other highly upregulated genes did not have any effect on cell growth. Brazilin may inhibit T24 cell growth and trigger cell death through a c-Fos-mediated and tumor cell specific signaling pathway. Further studies of its down stream mediators may help to identify better tumor cell type specific drug targets.

Brazilin selectively disrupts proximal IL-1 receptor signaling complex formation by targeting an IKK-upstream signaling components.[Pubmed:24735611]

Biochem Pharmacol. 2014 Jun 15;89(4):515-25.

The ligation of interleukin-1 receptor (IL-1R) or tumor necrosis factor receptor 1 (TNFR1) induces the recruitment of adaptor proteins and their concomitant ubiquitination to the proximal receptor signaling complex, respectively. Such are upstream signaling events of IKK that play essential roles in NF-kappaB activation. Thus, the discovery of a substance that would modulate the recruitment of key proximal signaling elements at the upstream level of IKK has been impending in this field of study. Here, we propose that Brazilin, an active compound of Caesalpinia sappan L. (Leguminosae), is a potent NF-kappaB inhibitor that selectively disrupts the formation of the upstream IL-1R signaling complex. Analysis of upstream signaling events revealed that Brazilin markedly abolished the IL-1beta-induced polyubiquitination of IRAK1 and its interaction with IKK-gamma counterpart. Notably, pretreatment of Brazilin drastically interfered the recruitment of the receptor-proximal signaling components including IRAK1/4 and TRAF6 onto MyD88 in IL-1R-triggerd NF-kappaB activation. Interestingly, Brazilin did not affect the TNF-induced RIP1 ubiquitination and the recruitment of RIP1 and TRAF2 to TNFR1, suggesting that Brazilin is effective in selectively suppressing the proximal signaling complex formation of IL-1R, but not that of TNFR1. Moreover, our findings suggest that such a disruption of IL-1R-proximal complex formation by Brazilin is not mediated by affecting the heterodimerization of IL-1R and IL-1RAcP. Taken together, the results suggest that the anti-IKK activity of Brazilin is induced by targeting IKK upstream signaling components and subsequently disrupting proximal IL-1 receptor signaling complex formation.

Induction of vasorelaxation through activation of nitric oxide synthase in endothelial cells by brazilin.[Pubmed:12729841]

Eur J Pharmacol. 2003 May 2;468(1):37-45.

The vasorelaxant activity of Caesalpinia sappan L., a traditional Chinese medicine, and its major component Brazilin were investigated in isolated rat aorta and human umbilical vein endothelial cells. In isolated rat aorta, C. sappan L. extract and Brazilin relaxed phenylephrine-induced vasocontraction and increased cyclic guanosine 3',5'-monophosphate (cGMP) content. Induction of vasorelaxation of Brazilin was endothelium-dependent and could be markedly blocked by pretreatment with nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME); N(G)-monomethyl-L-arginine acetate (L-NMMA) and guanylyl cyclase inhibitor, methylene blue; 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and nitric oxide (NO) scavenger, hemoglobin. The increasing cGMP content induced by Brazilin was also blocked by pretreatment with L-NAME, methylene blue, and the removal of extracellular Ca(2+). In human umbilical vein endothelial cells, Brazilin dose-dependently induced an increase in NO formation and NOS activity, which were greatly attenuated by either the removal of extracellular Ca(2+) or the chelating of intracellular Ca(2+) chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). Moreover, Brazilin dose-dependently induced the influx of extracellular Ca(2+) in human umbilical vein endothelial cells. Collectively, these results suggest that Brazilin induces vasorelaxation by the increasing intracellular Ca(2+) concentration in endothelial cells of blood vessels and hence activating Ca(2+)/calmodulin-dependent NO synthesis. The NO is released and then transferred into smooth muscle cells to activate guanylyl cyclase and increase cGMP content, resulting in vasorelaxation.

Brazilin isolated from Caesalpinia sappan L. inhibits rheumatoid arthritis activity in a type-II collagen induced arthritis mouse model.[Pubmed:25896410]

BMC Complement Altern Med. 2015 Apr 22;15:124.

BACKGROUND: Caesalpinia sappan L. extracts exhibit great therapeutic potential, and have been shown to have analgesic and anti-inflammatory properties. This study aimed to understand the anti-rheumatoid activity of Brazilin that was isolated from ethyl acetate extract of C. sappan L. The evaluations were conducted in mice with type-II collagen-induced arthritis (CIA). METHODS: Brazilin was purified via preparative HPLC and identified by mass spectrometry and 1H/13C NMR analysis. DBA/1J mice were divided into four groups (n=10). Three groups of mice received intradermal injections of inducer bovine type-II collagen (BTIIC; 2 mg/ml in 0.05 ml acetic acid) and 0.1 ml of booster complete Freund's adjuvant (CFA). A second injection of BTIIC with booster incomplete Freund's adjuvant (ICFA) was given subsequently after 21 days. On 22nd day, purified Brazilin (10 mg/kg body weight) or the disease-modifying anti-rheumatic drug methotrexate (3 mg/kg body weight) was administered intraperitoneally daily or every three days for 21 days, respectively to two groups of mice. At the 42nd day, mice sera were collected, and the levels of pro-inflammatory cytokines and stress enzyme markers in serum were measured using standard immunoassay methods. The microstructure and morphometric analyses of the bones were assessed using high-resolution microfocal computed tomography. RESULTS: Brazilin isolated from C. sappan reduced the arthritis index score and the extent of acute inflammatory paw edema in CIA-mice. The bone mineral density was significantly (p<0.05) lower in only-CIA mice, and appeared to increase commensurate with methotrexate and Brazilin administration. Brazilin prevented joint destruction, surface erosion, and enhanced bone formation as revealed by microstructural examinations. Brazilin markedly attenuated mouse CIA and reduced the serum levels of inflammatory cytokines including TNF-alpha, IL-1beta, and IL-6. CONCLUSIONS: Brazilin purified from C. sappan L. shows protective efficacy in CIA mouse, and may be useful to treat chronic inflammatory disorders including rheumatoid arthritis.

Brazilin inhibits UVB-induced MMP-1/3 expressions and secretions by suppressing the NF-kappaB pathway in human dermal fibroblasts.[Pubmed:22044921]

Eur J Pharmacol. 2012 Jan 15;674(2-3):80-6.

Brazilin (7, 11b-dihydrobenz[b]indeno[1,2-d]pyran-3,6a,9,10 (6H)-tetrol), the major component of Caesalpinia sappan L., is a natural red pigment used for histological staining. Recent studies have shown that Brazilin exhibits distinct biological effects, including anti-hepatotoxicity, antiplatelet activity, and anti-inflammatory activities. In the present study, we evaluated the effects of Brazilin on MMP-1 and -3 expressions in human dermal fibroblasts exposed to ultraviolet B (UVB) irradiation. Brazilin showed protective effect on UVB-induced loss of cell viability of fibroblasts. Brazilin also blocked significantly UVB-induced Reactive Oxygen Species generation in fibroblasts. Brazilin inhibited UVB-induced MMP-1/3 expressions and secretions in a dose-dependent manner. Moreover, UVB-induced NF-kappaB activation was completely blocked by treatment with Brazilin. These findings suggest that Brazilin inhibits UVB-induced MMP-1/3 expressions and secretions by suppressing of NF-kappaB activation in human dermal fibroblasts. Thus, Brazilin might be used as a potential agent for treatment of UV-induced skin photoaging.

Description

Brazilin is a red dye precursor obtained from the heartwood of several species of tropical hardwoods. Brazilin inhibits the cells proliferation, promotes apoptosis, and induces autophagy through the AMPK/mTOR pathway. Brazilin shows chondroprotective and anti-inflammatory activities.

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