OBJECTIVE: β-arrestin (ARRB2) is a member of arrestin family and a negative regulatory protein of G-coupling receptor, which is closely associated with the pathogenesis of several autoimmune diseases. This study aimed to investigate the mechanism of the effect of ARRB2 on the damage of human umbilical vein endothelial cells (HUVECs), which is induced by angiotensin II (Ang II). MATERIALS AND METHODS: ARRB2 at different concentration was used to interfere with the damage of HUVECs induced by Ang II or RNA interference technology to interfere with the expression of HUVECs followed by addition of Ang II to culture for 24 hours. Nitrate reduction method was used to measure the content of nitric oxide (NO) and radioimmunoassay was used to measure endothelin-1; Western blot assay was used to detect the expression of B-cell lymphoma-2 (Bcl-2), and flow cytometry was used to detect the intracellular level of reactive oxygen (ROS) and apoptosis of HUVECs. RESULTS: Our study found that ARRB2 could significantly reduce the generation and release of ROS, endothelin-1 (ET-1), lactic dehydrogenase (LDH) of HUVECs induced by Ang II and promote the generation of NO, superoxide dismutase (SOD) and scavenging in a dose-dependent manner. On the contrary, when expression of ARRB2 was disturbed by siRNA, increased generation and release of ROS, ET-1, and LDH were observed with reduced generation of NO, SOD and scavenging. In addition, ARRB2 could reverse the apoptosis of HUVECs induced by Ang II and was related to upregulate the expression of Bax. CONCLUSIONS: ARRB2 could protect the damage of HUVECs induced by Ang II and the mechanism was associated with upregulation of the expression of apoptosis and anti-apoptosis protein of Bcl-2.
OBJECTIVE: β-arrestin (ARRB2) is a member of arrestin family and a negative regulatory protein of G-coupling receptor, which is closely associated with the pathogenesis of several autoimmune diseases. This study aimed to investigate the mechanism of the effect of ARRB2 on the damage of human umbilical vein endothelial cells (HUVECs), which is induced by angiotensin II (Ang II). MATERIALS AND METHODS:ARRB2 at different concentration was used to interfere with the damage of HUVECs induced by Ang II or RNA interference technology to interfere with the expression of HUVECs followed by addition of Ang II to culture for 24 hours. Nitrate reduction method was used to measure the content of nitric oxide (NO) and radioimmunoassay was used to measure endothelin-1; Western blot assay was used to detect the expression of B-cell lymphoma-2 (Bcl-2), and flow cytometry was used to detect the intracellular level of reactive oxygen (ROS) and apoptosis of HUVECs. RESULTS: Our study found that ARRB2 could significantly reduce the generation and release of ROS, endothelin-1 (ET-1), lactic dehydrogenase (LDH) of HUVECs induced by Ang II and promote the generation of NO, superoxide dismutase (SOD) and scavenging in a dose-dependent manner. On the contrary, when expression of ARRB2 was disturbed by siRNA, increased generation and release of ROS, ET-1, and LDH were observed with reduced generation of NO, SOD and scavenging. In addition, ARRB2 could reverse the apoptosis of HUVECs induced by Ang II and was related to upregulate the expression of Bax. CONCLUSIONS:ARRB2 could protect the damage of HUVECs induced by Ang II and the mechanism was associated with upregulation of the expression of apoptosis and anti-apoptosis protein of Bcl-2.