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作 者:张宝红[1] 唐朝枢[2] 吴胜英[3] 杜军保[1]
机构地区:[1]北京大学第一医院儿科研究室,北京100034 [2]北京大学第一医院心血管研究所,北京100034 [3]郧阳医学院病理生理教研室,湖北十堰442000
出 处:《中国病理生理杂志》2003年第9期1157-1160,T001,共5页Chinese Journal of Pathophysiology
基 金:国家重点基础研究发展规划项目 (No .G2 0 0 0 0 5 6 90 5 )
摘 要:目的 :观察血管钙化时血管血红素加氧酶 (HO) -一氧化碳 (CO) -环磷酸鸟苷 (cGMP)系统的改变 ,以探讨血管钙化发病的细胞分子机理。方法 :利用维生素D3 (VitD3 )和尼古丁 (nicotine)复制大鼠血管钙化模型 ,检测HO - 1mRNA的相对含量 ,HO - 1免疫组织化学染色 ,测定主动脉HO - 1活性、碳氧血红蛋白 (HbCO)的生成及血管cGMP含量。结果 :用竞争性定量RT -PCR的方法发现 ,钙化动物血管组织的HO - 1mRNA水平较对照组低34 9% (P <0 0 5 ) ;免疫组织化学方法观察发现钙化血管的HO - 1蛋白表达减少 ,仅在内膜略有表达 ,中膜无明显表达 ;HO - 1活性低 6 0 6 % (P <0 0 1) ;CO生成少 5 3 9% (P <0 0 1) ,cGMP的含量低 77 1% (P <0 0 1)。结论 :钙化血管血红素 -HO -COAIM: To investigate the change of heme oxygenase (HO)-carbon monoxide (CO)-cyclic guanosine monophosphate (cGMP) pathway in vascular calcification, to clarify the cellular and molecular mechanimsm in vascular calcification.METHODS: Vascular calcification model was established in rats by using vitamin D 3 and nicotine. The relative content of HO-1 mRNA, immunochemistry (IH) for HO-1, HO activity, HbCO formation and content of cGMP in aorta were measured. RESULTS: Compared to those of control rats, the HO-1 mRNA level in vessels of rats in VDN group(vascular calcification group) were decreased by 34.9% ( P<0.05 ); expression of HO-1 protein were decreased too, there were trace positive staining of HO-1 in the endothelium, and no obvious immunoreactivity in the medial layer; HO-1 activity was decreased by 60.6% ( P<0.01 ), CO concentration was decreased by 53.9% ( P<0.01 ) and cGMP content was decreased by 77.1% ( P<0.01 ) in vessels of rats in VDN group. CONCLUSION: There were obvious down regulation in HO-CO-cGMP pathway in calcified vessels.
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