07.11.2014 Views

iv. mezioborové setkênè mladðch biologů ... - Chemické listy

iv. mezioborové setkênè mladðch biologů ... - Chemické listy

iv. mezioborové setkênè mladðch biologů ... - Chemické listy

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

Chem. Listy 98, 271 – 314 (2004) IV. Amerika 2004.<br />

complexes, promyeolocytic leukemia nuclear bodies (PML NBs).<br />

The gene product, PML protein, is essential for proper formation<br />

and integrity of PML NBs. Although the biochemical function of<br />

PML and PML NBs remain still unclear, there is an evidence for<br />

its contribution in response to a variety of cell states like cancer,<br />

apoptosis, and viral infections.<br />

It is known that type I and II interferons (IFNs)<br />

dramatically increase the transcription of the PML gene<br />

through an IFN-stimulated response elements (ISRE and GAS)<br />

present in the PML gene promoter. Additionally, IFNs<br />

increases expression of other structural component of PML<br />

NBs, Sp100, which is mediated by the same response<br />

elements. The up-regulation of these proteins, which are the<br />

main structural components of PML NBs, can contribute to the<br />

observed increase in the number of PML NBs.<br />

In this study we have shown that trichostatin A, an<br />

inhibitor of protein deacetylases, strongly reduces IFNstimulated<br />

increase of PML NBs number. Consistently with<br />

this observation, trichostatin A also inhibits IFN-induced upregulation<br />

of the main structural components of PML NBs –<br />

PML and Sp100. Although TSA-induced protein<br />

hyperacetylation has an overall stimulatory effect on gene<br />

expression, our findings indicate that the IFN-induced<br />

act<strong>iv</strong>ation of these two genes is inhibited at some stage by<br />

acetylation event of an unknown regulatory component.<br />

A BIOLOGICALLY ACTIVE COMPOUND FROM THE<br />

SEEDS OF Tamarindus indica<br />

M. VODENIČAROVÁ a , S. PÁVEK a , A. LOJEK b , and A.<br />

EBRINGEROVÁ c<br />

a CPN s.r.o., Dolní Dobrouč 56102, b Institute of Biophysics,<br />

Kralovopolska 135, 616 65 Brno, c Institute of Chemistry,<br />

Slovak Academy of Sciences, Dúbravska cesta 9, 842 38<br />

Bratislava, Slovak Republic<br />

vodenicarova@contipro.cz<br />

Tamarindus indica is a large tree growing in tropical and<br />

subtropical regions. It is one of the most important plant<br />

resources as food materials and all parts of the plant have<br />

therapeutic uses 1,2 . The germ obtained from the seed contains<br />

high molecular xyloglucan. Xyloglucan has an<br />

immunostimulating effect, but there was not obtained an<br />

antioxidat<strong>iv</strong>e act<strong>iv</strong>ity in alcoholic and water extract prepared<br />

from germ. Seed coats are a byproduct of tamarind gum<br />

production and are reported to be a low-cost source of<br />

antioxidants extractable with methanol, ethanol and<br />

ethylacetate. In these extracts, a variety of dihydroxy types of<br />

benzene der<strong>iv</strong>at<strong>iv</strong>es has been identified as the main<br />

component 3 .<br />

This study reports on the composition and general<br />

structural and molecular characteristics as well as various<br />

biological act<strong>iv</strong>ities of the compound isolated from the seed<br />

coats by aqueous alkali extraction and isopropanol extraction.<br />

The water – soluble alkali extracted material of tamarind seed<br />

coat (AEMTSC) comprises a high molecular mass heteroxylan<br />

(Mp ~ 90 kDa) closely associated with phenolic compounds. It<br />

exhibited significantly higher antioxidat<strong>iv</strong>e act<strong>iv</strong>ity as<br />

measured by total peroxyl radical trapping antioxidant<br />

parameter (TRAP) and DPPH radical scavenging method in<br />

comparison to isopropanol extract. The antioxidat<strong>iv</strong>e capacity<br />

is comparable with trolox. The reduction of phospholipid<br />

peroxidation in the presence of AEMTSC is more than 90 %<br />

for concentration of AEMTSC more than 0,05 % (wt.).<br />

AEMTSC is fully soluble in water and represents a potent<br />

natural addit<strong>iv</strong>e in cosmetic and pharmacy.<br />

REFERENCES<br />

1. Lanhers M. C., Fleurentin J., Guillemni F.:<br />

Ethnopharmacol. 18, 42 (1996).<br />

2. Shankaracharya N. B.: J. Food Sci. Technol. 35, 193<br />

(1998).<br />

3. Tsuda T., Watanabe M., Ohshima K., Yamamoto A.,<br />

Kawakishi S., Osawa T.: J. Agric. Food Chem. 42, 2671<br />

(1994).<br />

CHELERYTHRINE INHIBITION OF OXIDATIVE<br />

BURST IN DMSO-DIFFERENTIATED HL-60 CELLS<br />

PRECEDES PROTEIN KINASE C INHIBITION<br />

JIŘÍ VRBA and MARTIN MODRIANSKÝ<br />

Institute of Medical Chemistry and Biochemistry, Faculty of<br />

Medicine, Palacký Un<strong>iv</strong>ersity, Hněvotínská 3, 775 15 Olomouc<br />

Chelerythrine (CHE), a quaternary benzophenanthridine<br />

alkaloid with anti-inflammatory properties, is known to inhibit<br />

protein kinase C (PKC)-dependent phosphorylation. We<br />

examined the effect of CHE and three other alkaloids,<br />

sanguinarine (SA), dihydrosanguinarine (dihSA) and<br />

dihydrochelerythrine (dihCHE), on PKC-dependent oxidat<strong>iv</strong>e<br />

burst in DMSO-differentiated HL-60 cells. Phorbol myristate<br />

acetate (PMA) directly act<strong>iv</strong>ates PKC thus triggering NADPH<br />

oxidase assembly and oxidat<strong>iv</strong>e burst. Both CHE and SA<br />

inhibit PMA-induced oxidat<strong>iv</strong>e burst, monitored as superoxide<br />

radical generation, with IC50 of 2.9 µM and 1.8 µM,<br />

respect<strong>iv</strong>ely. Western blotting analyses of the whole cell lysate<br />

obtained from PMA-act<strong>iv</strong>ated differentiated HL-60 cells in the<br />

presence or absence of alkaloids showed that inhibition of<br />

PKC act<strong>iv</strong>ity required at least ten-fold higher concentrations of<br />

CHE (> 30 µM) or SA (> 20 µM) than those necessary for<br />

inhibition of PMA-induced superoxide generation.<br />

Staurosporine, a potent PKC inhibitor, inhibits both oxidat<strong>iv</strong>e<br />

burst and PKC act<strong>iv</strong>ity with comparable effect<strong>iv</strong>eness. DihSA<br />

and dihCHE at concentrations > 30 µM affected neither PMAinduced<br />

oxidat<strong>iv</strong>e burst nor PKC act<strong>iv</strong>ity. Comparison of<br />

effects displayed by CHE and SA with those displayed by their<br />

dihydro der<strong>iv</strong>at<strong>iv</strong>es accentuates the requirement for the<br />

presence of C=N+ region in the molecules, while slight<br />

difference in side chains seems to be inessential. As low<br />

concentrations of CHE do not affect the phosphorylating<br />

act<strong>iv</strong>ity of PKC, which directly act<strong>iv</strong>ates NADPH oxidase<br />

assembly via phosphorylation of p47 phox , we conclude that<br />

CHE inhibits oxidat<strong>iv</strong>e burst in DMSO-differentiated HL-60<br />

cells primarily by direct inhibition of NADPH oxidase.<br />

This research was supported by grant MSM 151100003.<br />

311

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!