Effects Of CaSR And Cbfα1on Calcified Vascular Smooth Muscle Cell In Yang Deficiency Of Spleen And Kidney Type Chronic Kidney Disease Stage5Patients

Objective:This study is aimed to explore the relationship between the expression of CaSR and Cbfal on calcified vascular smooth muscle cell in spleen deficiency type chronic kidney disease stage5patients and vascular cal calcification, and to explore a few basics of whether CaSR or Cbfal involved in vascular calcification and other plausible mechanism.Method:With Immunohistochemistry and the expression features of CaSR and Cbfal investigated by Western Blot, collect the basic information, medical history and inspection results and then calculate calcium-phosphorus product. Analyse the expression features and relationship between CaSR and Cbfal and the relationship between the expression of CaSR and Cbfal and other index and medical history.Using SPSS16.0statistic software to deal with data.Results:1, According to the results of immunohistochemistry and Western Blot, the expression of CaSR in CKD group saw an obvious decrease than normal group(.P<0.01);2, Immunohistochemistry and Western Blot test suggests that the expression of Cbfal in CKD group increased significantly than normal group(P<0.01);3,correlation analysis:there’s a negative correlation between the expression of CaSR and Cbfal(P<0.01), a positive correlation between the expression of Cbfal and peripheral blood phosphorus(P<0.01) and a negative correlation between the expression of CaSR and peripheral blood phosphorus(P<0.01) and a negative correlation between the expression of CaSR and calcium-phosphorus product (P<0.01).Conclusion:1, Hyperphosphatemia is an influential factor in the process of vascular angiosteosis and the expression of Cbfal is a significant symbol in the process.2, CaSR may play the role of protection in the process of vascular calcification of the patients with chronic kidney disease. In spleen deficiency type CKD patients CaSR expression reduce phosphorus levels elevated, CaSR inhibits calcification mechanism:through the activation of the ERK pathway protect VSMC from apoptosis, thereby reducing the release of the mineralized core factor, inhibit the transformation of VSMC to osteoblast-like phenotype; to maintain the level of calcium-phosphate product, to prevent calcium and phosphorus deposition in the form of bone salt of VSMC.