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| Plumbagin or 5-hydroxy-2-methyl-1,4-naphthoquinone is an organic compound with the chemical formula C11H8O3. It is regarded as a toxin and it is genotoxic and mutagenic.
Plumbagin is a yellow dye, formally derived from naphthoquinone.
It is named after the plant genus Plumbago, from which it was originally isolated.
It is also commonly found in the carnivorous plant genera Drosera and Nepenthes. It is also a component of the black walnut drupe. |
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Read full article at Wikipedia
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| InChI=1S/C11H8O3/c1-6-5-9(13)10-7(11(6)14)3-2-4-8(10)12/h2-5,12H,1H3 |
| VCMMXZQDRFWYSE-UHFFFAOYSA-N |
| CC1=CC(=O)C2=C(O)C=CC=C2C1=O |
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Plumbago scandens
(IPNI:30243613-2)
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Found in
root
(BTO:0001188).
See:
PubMed
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Plumbago rosea
(IPNI:687095-1)
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Found in
root
(BTO:0001188).
See:
DOI
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Plumbago europaea
(NCBI:txid114226)
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Found in
root
(BTO:0001188).
See:
DOI
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Nepenthes thorelii
(NCBI:txid122314)
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Found in
root
(BTO:0001188).
See:
PubMed
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Juglans nigra
(NCBI:txid16719)
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Found in
root
(BTO:0001188).
See:
PubMed
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Juglans nigra
(NCBI:txid16719)
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Found in
leaf
(BTO:0000713).
See:
PubMed
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Juglans nigra
(NCBI:txid16719)
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Found in
bark
(BTO:0001301).
See:
PubMed
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Juglans nigra
(NCBI:txid16719)
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Found in
xylem
(BTO:0001468).
Previous component: wood;
See:
PubMed
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Juglans regia
(NCBI:txid51240)
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Found in
xylem
(BTO:0001468).
Previous component: wood;
See:
PubMed
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Juglans regia
(NCBI:txid51240)
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Found in
leaf
(BTO:0000713).
See:
PubMed
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Juglans regia
(NCBI:txid51240)
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Found in
root
(BTO:0001188).
See:
PubMed
|
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Juglans regia
(NCBI:txid51240)
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Found in
bark
(BTO:0001301).
See:
PubMed
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Plumbago zeylanica
(NCBI:txid76149)
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Found in
root
(BTO:0001188).
See:
PubMed
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Juglans cinerea
(NCBI:txid91214)
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Found in
bark
(BTO:0001301).
See:
PubMed
|
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Juglans cinerea
(NCBI:txid91214)
|
Found in
xylem
(BTO:0001468).
Previous component: wood;
See:
PubMed
|
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Juglans cinerea
(NCBI:txid91214)
|
Found in
leaf
(BTO:0000713).
See:
PubMed
|
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Juglans cinerea
(NCBI:txid91214)
|
Found in
root
(BTO:0001188).
See:
PubMed
|
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metabolite
Any intermediate or product resulting from metabolism. The term 'metabolite' subsumes the classes commonly known as primary and secondary metabolites.
immunological adjuvant
A substance that augments, stimulates, activates, potentiates, or modulates the immune response at either the cellular or humoral level. A classical agent (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contains bacterial antigens. It could also be endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Its mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy is related to its antigen-specific immunoadjuvanticity.
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immunological adjuvant
A substance that augments, stimulates, activates, potentiates, or modulates the immune response at either the cellular or humoral level. A classical agent (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contains bacterial antigens. It could also be endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Its mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy is related to its antigen-specific immunoadjuvanticity.
anticoagulant
An agent that prevents blood clotting.
antineoplastic agent
A substance that inhibits or prevents the proliferation of neoplasms.
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View more via ChEBI Ontology
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5-hydroxy-2-methylnaphthalene-1,4-dione
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2-methyl-5-hydroxy-1,4-naphthoquinone
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ChemIDplus
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2-methyljuglone
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ChEBI
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5-hydroxy-2-methyl-1,4-naphthalenedione
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ChemIDplus
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5-hydroxy-2-methyl-1,4-naphthoquinone
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ChEBI
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plumbaein
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ChEBI
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Plumbagin
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KEGG COMPOUND
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plumbagine
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MetaCyc
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plumbagone
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ChEBI
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1870475
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Reaxys Registry Number
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Reaxys
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481-42-5
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CAS Registry Number
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KEGG COMPOUND
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481-42-5
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CAS Registry Number
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ChemIDplus
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959690
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Gmelin Registry Number
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Gmelin
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Lai L, Liu J, Zhai D, Lin Q, He L, Dong Y, Zhang J, Lu B, Chen Y, Yi Z, Liu M (2012)
Plumbagin inhibits tumour angiogenesis and tumour growth through the Ras signalling pathway following activation of the VEGF receptor-2.
British journal of pharmacology 165, 1084-1096 [PubMed:21658027]
[show Abstract]
Background and purposeAngiogenesis-based therapy is an effective anti-tumour strategy and previous reports have shown some beneficial effects of a naturally occurring bioactive compound plumbagin (5-hydroxy-2-methyl-1, 4-naphthoquinone). Here, we sought to determine the biological effects of plumbagin on signalling mechanisms during tumour angiogenesis.Experimental approachThe effects of plumbagin were evaluated in various in vitro assays which utilised human umbilical vein endothelial cells (HUVEC) proliferation, migration and tube formation. Plumbagin was also evaluated in vivo using chicken embryo chorioallantoic membrane (CAM) and mouse corneal micropocket models., Human colon carcinoma and prostate cancer xenograft mouse models were used to evaluate the effects of plumbagin on angiogenesis. Immunofluorescence, GST pull-down and Western blotting were employed to explore the underlying mechanisms of VEGF receptor (VEGFR)2-mediated Ras signalling pathways.Key resultsPlumbagin not only inhibited endothelial cell proliferation, migration and tube formation but also suppressed chicken chorioallantoic membrane neovascularzation and VEGF-induced mouse corneal angiogenesis. Moreover, plumbagin suppressed tumour angiogenesis and tumour growth in human colon carcinoma and prostate cancer xenograft mouse models. At a molecular level, plumbagin blocked the Ras/Rac/cofilin and Ras/MEK signalling pathways mediated by VEGFR2 in HUVECs.Conclusions and implicationsPlumbagin inhibited tumour angiogenesis and tumour growth by interference with the VEGFR2-mediated Ras signalling pathway in endothelial cells. Our findings demonstrate a molecular basis for the effects of plumbagin and suggest that this compound might have therapeutic ant-tumour effects. | Sun J, McKallip RJ (2011)
Plumbagin treatment leads to apoptosis in human K562 leukemia cells through increased ROS and elevated TRAIL receptor expression.
Leukemia research 35, 1402-1408 [PubMed:21741707]
[show Abstract]
This study examined the ability of plumbagin to induce apoptosis in chronic myelogenous leukemia (CML). Plumbagin exposure led to a significant reduction in cell viability and the induction of apoptosis. Mechanistically, plumbagin treatment led to elevated levels of ROS. Plumbagin-induced apoptosis was inhibited by N-acetyl L-cysteine (NAC) and PEG-catalase. Furthermore, plumbagin exposure led to elevated expression of DR4 and DR5 and increased killing through soluble TRAIL. The plumbagin-induced increase in DR4 and DR5 was inhibited by treatment with NAC. Together, this study suggests that plumbagin may be an effective treatment of CML through increased sensitivity to TRAIL-mediated killing. | Subramaniya BR, Srinivasan G, Sadullah SS, Davis N, Subhadara LB, Halagowder D, Sivasitambaram ND (2011)
Apoptosis inducing effect of plumbagin on colonic cancer cells depends on expression of COX-2.
PloS one 6, e18695 [PubMed:21559086]
[show Abstract]
Plumbagin, a quinonoid found in the plants of the Plumbaginaceae, possesses medicinal properties. In this study we investigated the anti-proliferative and apoptotic activity of plumbagin by using two human colonic cancer cell lines, HT29 and HCT15. IC50 of Plumbagin for HCT15 and HT29 cells (22.5 µM and 62.5 µM, respectively) were significantly different. To study the response of cancer cells during treatment strategies, cells were treated with two different concentrations, 15 µM, 30 µM for HCT15 and 50 µM, 75 µM for HT29 cells. Though activation of NFκB, Caspases-3, elevated levels of TNF-α, cytosolic Cytochrome C were seen in both HCT15 cells HT29 treated with plumbagin, aberrant apoptosis with decreased level of pEGFR, pAkt, pGsk-3β, PCNA and Cyclin D1was observed only in 15 µM and 30 µM plumbagin treated HCT15 and 75 µM plumbagin treated HT29 cells. This suggests that plumbagin induces apoptosis in both HCT15 cells and HT29 treated, whereas, proliferation was inhibited only in 15 µM and 30 µM plumbagin treated HCT15 and 75 µM plumbagin treated HT29 cells, but not in 50 µM plumbagin treated HT29 cells. Expression of COX-2 was decreased in 75 µM plumbagin treated HT29 cells when compared to 50 µM plumbagin treated HT29 cells, whereas HCT15 cells lack COX. Hence the observed resistance to induction of apoptosis in 50 µM plumbagin treated HT29 cells are attributed to the expression of COX-2. In conclusion, plumbagin induces apoptosis in colonic cancer cells through TNF-α mediated pathway depending on expression of COX-2 expression. | Xu KH, Lu DP (2010)
Plumbagin induces ROS-mediated apoptosis in human promyelocytic leukemia cells in vivo.
Leukemia research 34, 658-665 [PubMed:19748668]
[show Abstract]
Plumbagin, a naphtoquinone from the roots of Plumbago zeylanica is known to possess anticancer and anti-bacterial activity. Based on the former finding of our group in vitro demonstrating its effectiveness in human promyelocytic leukemia cells, NB4, in this study we further revealed the mitochondrial pathway involved in plumbagin-induced apoptosis. We also found that the generation of ROS was a critical mediator in plumbagin-induced apoptosis, which would be abrogated completely by antioxidant, NAC. The anticancer effect of plumbagin was investigated in vivo using NB4 tumor xenograft in NOD/SCID mice. The incidence of formation, growth characteristics, body weight and volume of tumors were observed. The histopathologic examination of tumors and organs were made. The results showed that intraperitoneal injection of plumbagin (2mg/kg body weight) daily for 3 weeks resulted to a 64.49% reduction of tumor volume compared with the control. Furthermore, there was no overt manifestation of toxicity such as weight loss, tissue damage and behavior change which appeared in Doxorubicin-treated mice (1mg/kg thrice a week). These results indicate that plumbagin has potential as a novel therapeutic agent for myeloid leukemia. | Luo P, Wong YF, Ge L, Zhang ZF, Liu Y, Liu L, Zhou H (2010)
Anti-inflammatory and analgesic effect of plumbagin through inhibition of nuclear factor-κB activation.
The Journal of pharmacology and experimental therapeutics 335, 735-742 [PubMed:20858709]
[show Abstract]
Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) (PL) is a naturally occurring yellow pigment found in the plants of the Plumbaginaceae, Droseraceae, Ancistrocladaceae, and Dioncophyllaceae families. It has been reported that PL exhibits anticarcinogenic, anti-inflammatory, and analgesic activities. However, the mechanism underlying its anti-inflammatory action remains unknown. In the current study, we investigated and characterized the anti-inflammatory and analgesic effects of PL orally administrated in a range of dosages from 5 to 20 mg/kg. We also examined the role of nuclear factor κB (NF-κB) and proinflammatory cytokines and mediators in this effect. The results showed that PL significantly and dose-dependently suppressed the paw edema of rats induced by carrageenan and various proinflammatory mediators, including histamine, serotonin, bradykinin, and prostaglandin E(2). PL reduced the number of writhing episodes of mice induced by the intraperitoneal injection of acetic acid, but it did not reduce the writhing episode numbers induced by MgSO(4) in mice or prolong the tail-flick reaction time of rats to noxious thermal pain. Mechanistic studies showed that PL effectively decreased the production of the proinflammatory cytokines interleukin 1β, interleukin 6, and tumor necrosis factor α. It also inhibited the expression of the proinflammatory mediators inducible nitric-oxide synthase and cyclooxygenase 2, whereas it did not inhibit the expression of cyclooxygenase 1. Further studies demonstrated that PL suppressed inhibitor of κBα phosphorylation and degradation, thus inhibiting the phosphorylation of the p65 subunit of NF-κB. This study suggests that PL has a potential to be developed into an anti-inflammatory agent for treating inflammatory diseases. | Aziz MH, Dreckschmidt NE, Verma AK (2008)
Plumbagin, a medicinal plant-derived naphthoquinone, is a novel inhibitor of the growth and invasion of hormone-refractory prostate cancer.
Cancer research 68, 9024-9032 [PubMed:18974148]
[show Abstract]
Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men. Hormone-refractory invasive PCa is the end stage and accounts for the majority of PCa patient deaths. We present here that plumbagin (PL), a quinoid constituent isolated from the root of the medicinal plant Plumbago zeylanica L., may be a potential novel agent in the control of hormone-refractory PCa. Specific observations are the findings that PL inhibited PCa cell invasion and selectively induced apoptosis in PCa cells but not in immortalized nontumorigenic prostate epithelial RWPE-1 cells. In addition, i.p. administration of PL (2 mg/kg body weight), beginning 3 days after ectopic implantation of hormone-refractory DU145 PCa cells, delayed tumor growth by 3 weeks and reduced both tumor weight and volume by 90%. Discontinuation of PL treatment in PL-treated mice for as long as 4 weeks did not result in progression of tumor growth. PL, at concentrations as low as 5 micromol/L, inhibited in both cultured PCa cells and DU145 xenografts (a) the expression of protein kinase Cepsilon (PKCepsilon), phosphatidylinositol 3-kinase, phosphorylated AKT, phosphorylated Janus-activated kinase-2, and phosphorylated signal transducer and activator of transcription 3 (Stat3); (b) the DNA-binding activity of transcription factors activator protein-1, nuclear factor-kappaB, and Stat3; and (c) Bcl-xL, cdc25A, and cyclooxygenase-2 expression. The results indicate for the first time, using both in vitro and in vivo preclinical models, that PL inhibits the growth and invasion of PCa. PL inhibits multiple molecular targets including PKCepsilon, a predictive biomarker of PCa aggressiveness. PL may be a novel agent for therapy of hormone-refractory PCa. | Sandur SK, Ichikawa H, Sethi G, Ahn KS, Aggarwal BB (2006)
Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) suppresses NF-kappaB activation and NF-kappaB-regulated gene products through modulation of p65 and IkappaBalpha kinase activation, leading to potentiation of apoptosis induced by cytokine and chemotherapeutic agents.
The Journal of biological chemistry 281, 17023-17033 [PubMed:16624823]
[show Abstract]
Plumbagin, derived from the medicinal plant Plumbago zeylanica, modulates cellular proliferation, carcinogenesis, and radioresistance, all known to be regulated by the activation of the transcription factor NF-kappaB, suggesting plumbagin might affect the NF-kappaB activation pathway. We found that plumbagin inhibited NF-kappaB activation induced by TNF, and other carcinogens and inflammatory stimuli (e.g. phorbol 12-myristate 13-acetate, H2O2, cigarette smoke condensate, interleukin-1beta, lipopolysaccharide, and okadaic acid). Plumbagin also suppressed the constitutive NF-kappaB activation in certain tumor cells. The suppression of NF-kappaB activation correlated with sequential inhibition of the tumor necrosis factor (TNF)-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 phosphorylation, p65 nuclear translocation, and the NF-kappaB-dependent reporter gene expression activated by TNF, TNFR1, TRAF2, NIK, IKK-beta, and the p65 subunit of NF-kappaB. Plumbagin also suppressed the direct binding of nuclear p65 and recombinant p65 to the DNA, and this binding was reversed by dithiothreitol both in vitro and in vivo. However, plumbagin did not inhibit p65 binding to DNA when cells were transfected with the p65 plasmid containing cysteine 38 mutated to serine. Plumbagin down-regulated the expression of NF-kappaB-regulated anti-apoptotic (IAP1, IAP2, Bcl-2, Bcl-xL, cFLIP, Bfl-1/A1, and survivin), proliferative (cyclin D1 and COX-2), and angiogenic (matrix metalloproteinase-9 and vascular endothelial growth factor) gene products. This led to potentiation of apoptosis induced by TNF and paclitaxel and inhibited cell invasion. Overall, our results indicate that plumbagin is a potent inhibitor of the NF-kappaB activation pathway that leads to suppression of NF-kappaB-regulated gene products. This may explain its cell growth modulatory, anticarcinogenic, and radiosensitizing effects previously described. | Hsieh YJ, Lin LC, Tsai TH (2005)
Determination and identification of plumbagin from the roots of Plumbago zeylanica L. by liquid chromatography with tandem mass spectrometry.
Journal of chromatography. A 1083, 141-145 [PubMed:16078700]
[show Abstract]
Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) is an herbal ingredient which is isolated from the root of Plumbago zeylanica L. This herb is a semi-climbing subshrub distributed in thickets or grassland at low elevations of Taiwan. The crushed roots of P. zeylanica L. were ground from lumps to powder and boiled with H2O, 50% EtOH, or 95% EtOH. Chromatographic separation of plumbagin from the herb was carried out using a ZORBAX Extend-C18 column (150 x 4.6 mm I.D.; 5 microm) that was eluted with the mobile phase of water-methanol (10:90, v/v). Multiple reaction monitoring (MRM) was used to monitor the transition of the deprotonated molecule m/z 187 [M-H]- to the product ion m/z 159 [M-H-CO]- for plumbagin analysis. The limit of quantification was determined to and accuracy of 1 ng/ml. Furthermore, the mass fractions of plumbagin in P. zeylanica L. for H2O, 50% EtOH and 95% EtOH were 0.24 +/- 0.04, 3.92 +/- 0.87 and 13.4 +/- 1.59 g/kg, respectively. These results present a reliable liquid chromatography coupled with tandem mass spectrometric (LC-MS/MS) method for the determination of plumbagin form herbal medicines. | Inbaraj JJ, Chignell CF (2004)
Cytotoxic action of juglone and plumbagin: a mechanistic study using HaCaT keratinocytes.
Chemical research in toxicology 17, 55-62 [PubMed:14727919]
[show Abstract]
Juglone (5-hydroxy-1,4-naphthoquinone) and plumbagin (5-hydroxy-3-methyl-1,4-naphthoquinone) are yellow pigments found in black walnut (Juglans regia). Herbal preparations derived from black walnut have been used as hair dyes and skin colorants in addition to being applied topically for the treatment of acne, inflammatory diseases, ringworm, and fungal, bacterial, or viral infections. We have studied the cytotoxicity of these quinones to HaCaT keratinocytes. Exposure to juglone or plumbagin (1-20 microM) resulted in a concentration-dependent decrease in cell viability. The cytotoxicity of these quinones is due to two different mechanisms, namely, redox cycling and reaction with glutathione (GSH). Redox cycling results in the generation of the corresponding semiquinone radicals, which were detected by electron paramagnetic resonance. Incubation of keratinocytes with the quinones generated hydrogen peroxide (H(2)O(2)) and resulted in the oxidation of GSH to GSSG. Depletion of GSH by buthionine sulfoximine enhanced semiquinone radical production, increased H(2)O(2) generation, and produced greater cytotoxicity, suggesting that GSH plays an important protective role. Both quinones decreased the intracellular levels of GSH. However, plumbagin stoichiometrically converted GSH to GSSG, indicating that redox cycling is its main metabolic pathway. In contrast, much of the GSH lost during juglone exposure, especially at the higher concentrations (10 and 20 microM), did not appear as GSSG, suggesting that the cytotoxicity of this quinone may also involve nucleophilic addition to GSH. Our findings indicate that topical preparations containing juglone and plumbagin should be used with care as their use may damage the skin. However, it is probable that the antifungal, antiviral, and antibacterial properties of these quinones are the result of redox cycling. | de Paiva SR, Figueiredo MR, Aragão TV, Kaplan MA (2003)
Antimicrobial activity in vitro of plumbagin isolated from Plumbago species.
Memorias do Instituto Oswaldo Cruz 98, 959-961 [PubMed:14762525]
[show Abstract]
Plumbagin is a naturally occurring naphthoquinone isolated from roots of Plumbago scandens. The plant was collected at the Campus of Fundação Oswaldo Cruz, Rio de Janeiro, Brazil. P. scandens is used as a traditional medicine for the treatment of several diseases. The antimicrobial activity of plumbagin was evaluated using the macrodilution method. The compound exhibited relatively specific activity against bacteria and yeast. The minimum inhibitory concentration test showed the growth inhibiton of Staphylococcus aureus at a concentration of 1.56 g/ml and of Candida albicans at a concentration of 0.78 g/ml. These results suggest the naphthoquinone plumbagin as a promising antimicrobial agent. |
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