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Tytuł pozycji:

Tongxinluo Inhibits Cyclooxygenase-2, Inducible Nitric Oxide Synthase, Hypoxia-inducible Factor-2α/Vascular Endothelial Growth Factor to Antagonize Injury in Hypoxia-stimulated Cardiac Microvascular Endothelial Cells

Tytuł :
Tongxinluo Inhibits Cyclooxygenase-2, Inducible Nitric Oxide Synthase, Hypoxia-inducible Factor-2α/Vascular Endothelial Growth Factor to Antagonize Injury in Hypoxia-stimulated Cardiac Microvascular Endothelial Cells
Autorzy :
Yan-Ning Li
Xiu-Juan Wang
Bin Li
Kun Liu
Jin-Sheng Qi
Bing-Hui Liu
Ye Tian
Pokaż więcej
Temat :
Cyclooxygenase-2
Hypoxia-inducible Factor-2α
Hypoxia
Inducible Nitric Oxide Synthase
Tongxinluo
Vascular Endothelial Growth Factor
Medicine
Źródło :
Chinese Medical Journal, Vol 128, Iss 8, Pp 1114-1120 (2015)
Wydawca :
Wolters Kluwer, 2015.
Rok publikacji :
2015
Kolekcja :
LCC:Medicine
Typ dokumentu :
article
Opis pliku :
electronic resource
Język :
English
ISSN :
0366-6999
Relacje :
http://www.cmj.org/article.asp?issn=0366-6999;year=2015;volume=128;issue=8;spage=1114;epage=1120;aulast=Li; https://doaj.org/toc/0366-6999
DOI :
10.4103/0366-6999.155119
Dostęp URL :
https://doaj.org/article/e0d7851d466a4cf896d592c8d298ea1a
Numer akcesji :
edsdoj.0d7851d466a4cf896d592c8d298ea1a
Czasopismo naukowe
Background: Endothelial dysfunction is considered as the initiating process and pathological basis of cardiovascular disease. Cyclooxygenase-2 (COX-2) and prostacyclin synthase (PGIS), inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) are key enzymes with opposing actions in inflammation and oxidative stress, which are believed to be the major driver of endothelial dysfunction. And in hypoxia (Hx), Hx-inducible factor (HIF)-1α and HIF-2α are predominantly induced to activate vascular endothelial growth factor (VEGF), resulting in abnormal proliferation. Whether and how Tongxinluo (TXL) modulates COX-2, PGIS, iNOS, eNOS, HIF-1α, HIF-2α, and VEGF in Hx-stimulated human cardiac microvascular endothelial cells (HCMECs) have not been clarified. Methods: HCMEC were treated with CoCl 2 to mimic Hx and the mRNA expressions of COX-2, PGIS, iNOS, eNOS, HIF-1α, HIF-2α, and VEGF were first confirmed, and then their mRNA expression and protein content as well as the cell pathological alterations were evaluated for TXL treatment with different concentrations. In addition, the effector molecular of inflammation prostaglandin E 2 (PGE 2 ) and the oxidative marker nitrotyrosine (NT) was adopted to reflect HCMEC injury. Results: Hx could induce time-dependent increase of COX-2, iNOS, HIF-2α, and VEGF in HCMEC. Based on the Hx-induced increase, TXL could mainly decrease COX-2, iNOS, HIF-2α, and VEGF in a concentration-dependent manner, with limited effect on the increase of PGIS and eNOS. Their protein contents verified the mRNA expression changes, which was consistent with the cell morphological alterations. Furthermore, high dose TXL could inhibit the Hx-induced increase of PGE 2 and NT contents, attenuating the inflammatory and oxidative injury. Conclusions: TXL could inhibit inflammation-related COX-2, oxidative stress-related iNOS, and HIF-2α/VEGF to antagonize Hx-induced HCMEC injury.

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