• Natural Product Sciences
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• v.21 no.4
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• pp.255-260
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• 2015

Two new thiodiketopiperazines (TDKPs), designated graphiumins I (1) and J (2), were isolated from the culture broth of the marine-derived fungus Graphium sp. OPMF00224 by solvent extraction, silica gel column chromatography, and HPLC. Their absolute structures were elucidated by spectroscopic analyses (1D and 2D NMR data, ROESY correlations, and CD data) and chemical methods. They were found to be structurally rare TDKPs with a phenylalanine-derived indolin substructure. Compounds 1 and 2 inhibited yellow pigment production by methicillin-resistant Staphylococcus aureus (MRSA) with $IC_{50}$ values of 63.5 and $76.5{\mu}g/ml$, respectively, without inhibiting its growth, even at $250{\mu}g/ml$.

• Journal of Life Science
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• v.18 no.9
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• pp.1219-1224
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• 2008

The embryonic zebrafish (Danio rerio) is rapidly becoming an important model organism for studies of early events in vertebrate development. Neural crest-derived pigment cell precursors of the embryonic zebrafish give rise to melanophores, xanthophores, and/or iridophores. Cell-signaling mechanisms related to the development of pigmentation and pigment pattern formation remain obscure. In this study, zebrafish embryos were treated with various signaling-related molecules - LiCl (an inositol-phosphatase inhibitor), forskolin (a protein kinase-A activator), a combination of LiCl/forskolin, and LiCl/heparin (an IP3 inhibitor) in order to identify the mechanisms involved in pigmentation. LiCl treatment resulted in ultrastructural and morphological alterations of melanophores. To identify the possible proteins responsible for this ultrastructural and morphological change, phosphorylation patterns in vitro and in vivo were analyzed. LiCl and LiCl/forskolin treatment elicited dramatic increases in the phosphorylation of a 55-kDa protein which was inhibited by heparin treatment. LiCl treatment also induced phosphorylation of a 55-kDa protein in melanophores purified from adult zebrafish. Collectively these results suggest that a LiCl-induced 55-kDa phosphoprotein plays a role in melanophore morphology and ultrastructure and ultimately effects gross pigmentation.

• BMB Reports
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• v.34 no.3
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• pp.189-193
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• 2001

Curcumin a yellow pigment from Curcuma Tonga, has been known to possess antioxidative and anticarcinogenic properties, as well as to induce apoptosis in some cancer cells. There have been, however, several contradictory reports that hypothesized curcumin (a hydrophobic molecule) can bind a membrane Gpid bilayer and induce nonspecific cytotoxicity in some cell lines. Why curcumin shows these contradictory effects is unknown. In A-431 cells, growth inhibition by curcumin is due mostly to the specific inhibition of the intrinsic tyrosine kinase activity of the epidermal growth factor receptor, as reported earlier by Korutla et al. Thus, we assumed that the cell death of A-431 by curcumin might be due to the specific induction of apoptosis. In this paper we clearly show that curcumin induces apoptosis in A-431 cells. The cureumin-induced cell death of A-431 exhibited various apoptotic features, including DNA fragmentation and nuclear condensation. Furthermore, the curcumin-induced apoptosis of A-431 cells involved activation of caspase-3-like cysteine protease. Involvement of caspase-3 was further confirmed by using a caspase-3 specific inhibitor, DEVD-CHO. In another study, decreased nitric oxide (NO) production was also shown in A-431 cells treated with curcumin, which seems to be the result of the inhibition of the iNOS expression by curcumin, as in other cell lines. However, 24 h after treatment of curcumin there was increased NO production in A-431 cells. This observation has not yet been clearly explained. We assumed that the increased NO production may be related to denitrosylation of the enzyme catalytic site in caspase-3 when activated. Taken together, this study shows that the cell death of A-431 by curcumin is due to the induction of apoptosis, which involves caspase-3 activation.