Diethyl citrate reduces the oxidative stress level in CRF vascular calcification through CaSR / 西安交通大学学报(医学版)

ABSTRACT

Objective To investigate the inhibitory effects and mechanisms of diethyl citrate (Et2Cit) on oxidative stress and vascular calcification in chronic renal failure (CRF). Methods SD rats were divided into four groups control group, model group, Et2Cit group and Et2Cit+NPS2143 (calcium sensitive receptor inhibitors) group. Alizarin red staining was used to detect aortic calcification in CRF rats. Concentrations of superoxide dismutase (SOD) and nitric oxide (NO) in the aorta and plasma of CRF rats were measured. The cells were divided into four groups control group, high-phosphorus group, Et2Cit group, and Et2Cit+NPS2143 group. The levels of dihydroethidium (DHE) and reactive oxygen species (ROS) were detected by flow cytometry. Results Compared with that in the control group, the aortic calcification degree in the model group was significantly increased. Et2Cit intervention could reduce the aortic calcification level. Aorta and plasma SOD and NO contents in the model group were significantly decreased (P<0.05). Et2Cit intervention could increase SOD and NO contents in the aorta and plasma (P<0.05). However, when NPS2143 and Et2Cit were given simultaneously, the effect of Et2Cit in improving vascular calcification and oxidative stress levels were inhibited (P<0.05). DHE and ROS levels were increased in cells under high phosphorus environment (P<0.05), and Et2Cit intervention could decrease DHE and ROS levels (P<0.05). However, compared with Et2Cit group, DHE and ROS levels in Et2Cit+NPS2143 group were increased (P<0.05). Conclusion Et2Cit inhibited oxidative stress level in CRF vascular calcification, which is dependent on calcium-sensitive receptors.