Aqueous Fraction from Aerial Parts Attenuates Angiotensin II-Induced Endothelial Dysfunction In Vivo by Activating Akt.

Background: Endothelial dysfunction (ED) is a marker of vascular damage and a precursor of cardiovascular diseases such as hypertension, which involve inflammation and organ damage. Nitric oxide (NO), produced by eNOS, which is induced by pAKT, plays a crucial role in the function of a healthy endothelium.

Methods: A combination of subfractions SF1 and SF3 (C4) of the aqueous fraction from (Cs-Aq) was evaluated to control endothelial dysfunction in vivo and on HMEC-1 cells to assess the involvement of pAkt in vitro.

Characterization of a murine model of endothelial dysfunction induced by chronic intraperitoneal administration of angiotensin II.

Endothelial dysfunction (ED) is a key factor for the development of cardiovascular diseases. Due to its chronic, life-threatening nature, ED only can be studied experimentally in animal models. Therefore, this work was aimed to characterize a murine model of ED induced by a daily intraperitoneal administration of angiotensin II (AGII) for 10 weeks.

An early lesion of the lateral septal nuclei produces changes in the forced swim test depending on gender.

1. Several pharmacological maneuvers in very young rats produce later changes resembling human depression. 2.