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本文旨在观察钙化细胞血红素加氧酶 (HO) -一氧化碳 (CO) -环磷酸鸟苷 (cGMP)系统的改变 ,以探讨血管钙化发生的细胞分子机理。利用 β 甘油磷酸制备钙化血管平滑肌细胞 (VSMCs) ,测定细胞钙含量、碱性磷酸酶活性及4 5Ca沉积 ;观察HO 1免疫细胞化学染色 ;测定VSMCsHO 1活性、碳氧血红蛋白 (HbCO)的生成及cGMP含量。发现钙化细胞的钙含量、碱性磷酸酶活性及4 5Ca沉积均比正常组显著升高。钙化细胞HO 1的表达不均匀 ,钙化结节中HO 1表达强于正常细胞。与正常平滑肌细胞相比 ,钙化细胞的HO 1活性低 4 2 7% [36 4± 2 8pmol (mgprotein·h)vs 6 3 5± 5 3pmol (mgprotein·h) ,P <0 0 1];CO含量低 39 2 % (3 38± 0 39μmol mgproteinvs 5 5 6± 0 4 8μmol mgprotein ,P <0 0 5 ) ;cGMP含量比正常细胞低 78 1% (4 3± 0 5vs 19 6± 1 2pmol mgprotein ,P <0 0 1)。提示钙化血管血红素 HO CO cGMP途径功能下调
This article aims to observe changes of heme oxygenase (HO) - carbon monoxide (CO) - cyclic guanosine monophosphate (cGMP) system in calcified cells in order to investigate the cellular molecular mechanism of vascular calcification. Calculated vascular smooth muscle cells (VSMCs) were prepared by β-glycerophosphate, and the contents of calcium, alkaline phosphatase and 4 5Ca were measured. Immunocytochemical staining of HO 1 was performed. The activity of HO 1, the formation of carboxyhemoglobin (HbCO) cGMP content. Calcium content, alkaline phosphatase activity and 4 5Ca deposition in calcified cells were significantly higher than those in normal group. The expression of HO 1 in calcified cells was uneven, and the expression of HO 1 in calcified nodules was stronger than that in normal cells. Compared with normal smooth muscle cells, the calcified cells had a lower HO 2 activity of 42.7% (36 4 ± 2 8 pmol (mg protein · h) vs 6 3 5 ± 5 3 pmol (mg protein · h), P <0.01), CO The content of cGMP was 39 2% lower than that of normal cells (3 38 ± 0 39 μmol mgprotein vs 5 56 ± 0 48 μmol mgprotein, P <0.05), and the cGMP content was 78 1% lower than that of normal cells (43 ± 0 5 vs 19 6 ± 1 2 pmol mgprotein, P <0 0 1). Tip calcification vascular heme HO CO cGMP pathway function down