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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 688
The 62nd National Congress of the Italian Physiological Society
9/25/2011-9/27/2011
Sorrento, Italy


ENDOTHELIAL DYSFUNCTION: ROS/RNS PRODUCTION , OXIDATIVE STRESS AND CATECHINS IN HYPERTHERMIA IN HUVECS
Abstract number: O18

CARINO1 AR, COSTANZO1 S, BRUNO2 R, MARTINO1 G

1Dept Cell Biology, Calabria Univ., Rende, Italy
2Dept Pharmaco-Biology, Calabria Univ., Rende, Italy

Background: 

Catechin possesses highly antihypertensive properties and is studied to use it in vitro since it prevents oxidative stress-induced by endothelial dysfunction. The aim of this work is to examine the role of the reactive oxygen and nitric oxide species (ROSs/RNSs) in the damage induced by hyperthermia in HUVECs with or without the interaction of Angiotensin II and AT1R, AT2R antagonists (Losartan and PD123319) in presence of Catechin.

Materials and Methods: 

Authors evaluated the Cathechin action( 50 mM final concentration in vitro) with or without addition of Angiotensin II, Losartan, PD123,319 both in normal and in treated cells also in long times culture (1-3-7 days). After physical treatment at a temperatures of 40-41° HUVECs were incubated with different kind of dyes: Acridine Orange (viability test), 2¹7¹- diclorodiidrofluoresceina diacetate to evaluate ROS production, DAF-2DA to analyze NO formation and Propidium Iodide to test molecular damages of nuclear DNA. Data analysis were captured by Cell-A program on Olympus IX 50 inverted microscope and intensity of fluorescence was measured by NIH Image J programs v.1.60 image analysis program.

Results: 

Hyperthermia increases proliferation in samples treated with Ang II at 1-3- 7 days and in samples treated with Cathechin. It decreases the ROS production levels for the samples treated with Cathechin and in those treated with Ang II, PD123319 and Catechin. NO levels are modulated by presence of Cathechin by AT1R pathway, also nuclear damages on DNA are modulated by Catechin action in hyperthermic samples.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 688 :O18

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