Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1
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Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2013, vol. 22, nr 6, November-December, p. 795–800

Publication type: original article

Language: English

The Effect of Valdecoxib on the Production of Growth Factors Evoked by Hypoxia and Bacterial Lipopolysaccharide in HMEC-1 Cells

Wpływ waldekoksybu na wydzielanie czynników wzrostu wywołane hipoksją i bakteryjnym lipopolisacharydem w komórkach HMEC-1

Anna Wiktorowska-Owczare1,K

1 Department of Pharmacology, Chair of Pharmacology and Clinical Pharmacology, Medical University of Lodz, Poland

Abstract

Background. Endothelial cells produce prostaglandins (PGE2 and PGI2) and growth factors (VEGF and bFGF). These substances regulate proliferation of cells, inflammatory processes and neovascularization under physiological and pathological conditions.
Objectives. The aim of this study was to check whether valdecoxib – a selective COX-2 inhibitor – inhibits VEGF and/or bFGF secretion in the presence of LPS or cobalt chloride in normal human microvascular endothelial cells (HMEC-1).
Material and Methods. HMEC-1 cells were treated with valdecoxib at a concentration of 10 and 100 µM in the presence of 100 µg/mL LPS or 200 µM CoCl2. The effect of NSAIDs and LPS on VEGF and bFGF proteins was analyzed by ELISA kit (R&D Systems). Cell viability was measured using the 3-[4.5-dimethylthiazol-2-yl]-2.5- -diphenyltetrazolium bromide (MTT) method.
Results. Valdecoxib inhibited LPS-induced proliferation of endothelial cells and bFGF secretion in a dose-dependent manner. Valdecoxib stimulated VEGF formation via HMEC-1 under inflammatory conditions.
Conclusion. Ultimately, the anti-angiogenic effect of the selective COX-2 inhibitor was a result of inhibition of HMEC-1 cell proliferation and bFGF generation under inflammatory conditions

Streszczenie

Wprowadzenie.Komórki śródbłonka wytwarzają prostaglandyny (PGE2 i PGI2) i czynniki wzrostu (VEGF i bFGF). Te substancje regulują proliferację komórek, proces zapalny oraz neowaskularyzację w warunkach fizjologicznych i patologicznych.
Cel pracy. Sprawdzenie czy waldekoksyb – selektywny COX-2 inhibitor hamuje wydzielanie VEGF i/lub bFGF w obecności LPS lub chlorku kobaltu w linii komórkowej śródbłonka HMEC-1.
Materiał i metody. Komórki HMEC-1 były inkubowane z waldekoksybem w stężeniach 10 i 100 µM w obecności 100 µg/ml LPS lub 200 µM CoCl2. Efekt NLPZ-tu i LPS na wydzielanie VEGF i bFGF był analizowany za pomocą ELISA kitu (R & D system). Żywotność komórek była mierzona testem MTT.
Wyniki. Waldekoksyb zahamował proliferację komórek śródbłonka indukowaną LPS oraz wydzielanie bFGF w sposób zależny od dawki. Jednocześnie waldekoksyb pobudzał tworzenie VEGF przez HMEC-1 w warunkach zapalenia.
Wnioski. Ostatecznie antyangiogenne działanie selektywnego inhibitora COX-2 było rezultatem zahamowania proliferacji komórek HMEC-1 i tworzenia bFGF w warunkach zapalenia

Key words

LPS, VEGF, bFGF, valdecoxib, endothelial cells.

Słowa kluczowe

LPS, VEGF, bFGF, waldekoksyb, komórki śródbłonka.

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