Yellow needle shape crystal
Juglans regia L./Occurs in Juglans spp.; leaves and nuts of pecan (Carya illinoensis), leaves of Pterocarya fraxinifolia, Lomatia spp. and Platycarya strobilacea. Also prod. by Penicillium diversum var. aureum and a mutant of Verticillium dahliae
Nucin/Juglone/5-Hydroxy-1,4-naphthalenedione/C.I. Natural Brown 7/5-hydroxynaphthalene-1,4-dione/Regianin/CI 75500/5-hydroxy-1,4-dihydronaphthalene-1,4-dione/5-Hydroxy-1,4-naphthochinone/1,4-Naphthalenedione, 5-hydroxy-/5-HNQ/5-Hydroxy-p-naphthoquinone/5-Hydroxy-1,4-naphthoquinone
385.8±42.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:481-39-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Juglone (5-hydroxyl-1,4-naphthoquinone) is a phenolic compound found in walnuts. Because of the antioxidant capacities of phenolic compounds, juglone may serve to combat oxidative stress, thereby protecting against the development of various diseases and aging processes. However, being a quinone molecule, juglone could also act as a redox cycling agent and produce reactive oxygen species. Such prooxidant properties of juglone may confer health effects, such as by killing cancer cells. Further, recent studies revealed that juglone influences cell signaling. Notably, juglone is an inhibitor of Pin1 (peptidyl-prolyl cis/trans isomerase) that could regulate phosphorylation of Tau, implicating potential effects of juglone in Alzheimer’s disease. Juglone also activates mitogen-activated protein kinases that could promote cell survival, thereby protecting against conditions such as cardiac injury. This review describes recent advances in the understanding of the effects and roles of juglone in oxidative stress and cell signaling.
Pin1; antioxidants; juglone; naphthoquinone; redox; signal transduction; walnuts
Juglone in Oxidative Stress and Cell Signaling.
Ahmad T1, Suzuki YJ2.
2019 Apr 5
Myeloid-derived suppressor cells (MDSCs) contribute to immune activity suppression and promote the tumor progression. Elimination of MDSCs is a promising cancer therapeutic strategy, and some chemotherapeutic agents have been reported to hamper tumor progression by suppressing MDSCs. Juglone has been showed to exert a direct cytotoxic effect on tumor cells. However, the effect of juglone on MDSCs and anti-tumor immune statue has remained unexplored. In our study, we observed that juglone suppressed tumor growth and metastasis markedly, and the tumor growth suppression in immunocompetent mice was more drastic than that in immunodeficient mice. Juglone reduced the accumulation of MDSCs and increased IFN-γ production by CD8+ T cells. Consistently, juglone affected myeloid cells differentiation and maturation, impairing the immunosuppressive functions of MDSCs. Moreover, juglone down-regulated the level of IL-1β which was mediating accumulation of MDSCs. In addition, juglone inhibited 5FU-induced liver injury in a colorectal carcinoma-bearing mice model. Thus, our work suggests that the anti-tumor effect of juglone is mediated, at least in part, by eliminating accumulation of MDSCs.
Copyright ? 2019 Elsevier B.V. All rights reserved.
CD8(+) T cells; IL-1β; Juglone; Myeloid derived suppressor cells (MDSCs)
Juglone eliminates MDSCs accumulation and enhances antitumor immunity.
Wang H1, Zou C1, Zhao W1, Yu Y1, Cui Y1, Zhang H1, E F1, Qiu Z1, Zou C2, Gao X3.
Accumulating data show that prolylisomerase (Pin1) is overexpressed in human glioblastoma multiforme (GBM) specimens. Therefore, Pin1 inhibitors should be investigated as a new chemotherapeutic drug that may enhance the clinical management of human gliomas. Recently, juglone, a Pin1 inhibitor, was shown to exhibit potent anticancer activity in various tumor cells, but its role in human glioma cells remains unknown. In the present study, we determined if juglone exerts antitumor effects in the U251 human glioma cell line and investigated its potential underlying molecular mechanisms. Cell survival, apoptosis, migration, angiogenesis and molecular targets were identified with multiple detection techniques including the MTT cell proliferation assay, dual acridine orange/ethidium bromide staining, electron microscopy, transwell migration assay, chick chorioallantoic membrane assay, quantitative real-time polymerase chain reaction and immunoblotting. The results showed that 5-20 ?M juglone markedly suppressed cell proliferation, induced apoptosis, and enhanced caspase-3 activity in U251 cells in a dose- and time-dependent manner. Moreover, juglone inhibited cell migration and the formation of new blood vessels. At the molecular level, juglone markedly suppressed Pin1 levels in a time-dependent manner. TGF-β1/Smad signaling, a critical upstream regulator of miR-21, was also suppressed by juglone. Moreover, the transient overexpression of Pin1 reversed its antitumor effects in U251 cells and inhibited juglone-mediated changes to the TGF-β1/miR-21 signaling pathway. These findings suggest that juglone inhibits cell growth by causing apoptosis, thereby inhibiting the migration of U251 glioma cells and disrupting angiogenesis; and that Pin1 is a critical target for juglone’s antitumor activity. The present study provides evidence that juglone has in vitro efficacy against glioma. Therefore, additional studies are warranted to examine the clinical potential of juglone in human gliomas.
Juglone reduces growth and migration of U251 glioblastoma cells and disrupts angiogenesis.
Wang J1, Liu K2, Wang XF2, Sun DJ3.