Channel: Basic Research http://journal23.magtechjournal.com/Jwk3_gjyyws EN-US http://journal23.magtechjournal.com/Jwk3_gjyyws/EN/1007-1245/current.shtml http://journal23.magtechjournal.com/Jwk3_gjyyws 1007-1245 http://journal23.magtechjournal.com/Jwk3_gjyyws/EN/10.3760/cma.j.issn.1007-1245.2021.06.019 Objective To investigate the effect of sodium citrate (Na₃Cit) on calcification of vascular smooth muscle cells (MOVAS) in mice with chronic kidney disease (CKD) induced by high phosphorus and its mechanism, and to search for drugs that are anticoagulant and can improve vascular calcification (VC) of CKD. Methods MOVAS was cultured in high phosphorus and different concentrations of Na₃Cit for 14 days. Calcium deposition was detected by alizarin red staining and o-cphenolphthalein complex ketone method; phenotype transformation was detected by real-time fluorescent quantitative PCR and alkaline phosphatase (ALP) staining; apoptosis was detected by annexin V staining. Results Na₃Cit significantly inhibited the calcification of CKD MOVAS induced by high phosphorus, and the inhibitory effect of high concentration of Na₃Cit was better. Na₃Cit could inhibit calcium and phosphorus deposition by forming calcium citrate chelate, thus inhibiting calcification. Na₃Cit could also inhibit ALP activity and up-regulate SM22-α expression of smooth muscle cells under high phosphorus conditions, thus preventing smooth muscle cells from differentiating into osteoblast like phenotype; meanwhile, it could reduce apoptosis induced by high phosphorus to inhibit calcification. Conclusion Na₃Cit can effectively reduce the calcification of MOVAS induced by high phosphorus. As a blood anticoagulant, Na₃Cit may play an anti VC role in clinic.]]>