LAUSR

Abstract Background: Henoch-Schonlein purpura (HSP) is a common hemorrhagic disease, which manifests the inflammation in the body's most microvasculars. Angiotensin II (Ang II) can induce the damage and apoptosis of vascular endothelial cells while angiotensin converting enzyme 2 (ACE2) can antagonist the action of Ang II. However, the effect of ACE2 on Ang II-induced endothelial damage remains unknown. Objective: To evaluate the effect of recombinant human angiotensin converting enzyme 2 (rhACE2) on the Ang II-induced damage of human umbilical vein endothelial cells (HUVECs) and the release of inflammatory mediator in vitro. Methods: Cultured HUVECs were randomly divided into 6 groups: the control group, rhACE2 group, Ang II group, and Ang II+ rhACE2 groups (3 subgroups). The cell vitality, cell cycle, apoptosis rate of the HUVECs and the levels of reactive oxygen species (ROS), interleukin 8 (IL-8), tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) and lactate dehydrogenase (LDH) were measured, respectively. Results: Compared with the control group, the cell viability and the rate of S phase cells in Ang II group significantly decreased (P < .05) while the apoptosis percentage and the levels of ROS, IL-8, TNF-α, TGF-β1, and LDH in Ang II group significantly increased (P < .05). There were no significant differences between the control group and rhACE2 group. Compared with the Ang II group, the cell viability and the rate of S phase cells in Ang II+rhACE2 groups were higher (P < .05) and the apoptosis percentage, the level of ROS, IL-8, TNF-α, TGF-β1, LDH in Ang II+rhACE2 groups were lower (P < .05). Conclusions: Ang II can induce the apoptosis of HUVECs and the release of inflammatory mediator, while rhACE2 can inhibit the detrimental effects of Ang II. The results of this study suggest that rhACE2 has a protective effect on HSP, which is probably a new way for the prevention and treatment of HSP.