心血管组织钙化时内源性硫化氢系统下调

目的：观察心血管组织钙化时内源性硫化氢生成系统(CSE/H2S)的变化，以探讨内源性硫化氢在心血管组织钙化中的作用及血管钙化的细胞分子机制。方法：在维生素D3 (Vit D3)和尼古丁(nicotine)诱导大鼠血管钙化模型上，测定钙含量、［45Ca2+］沉积及碱性磷酸酶（ALP）活性判断心血管钙化程度,采用生化法测定血浆、心肌组织和主动脉H2S含量及CSE活性，半定量RT-PCR方法测定心血管组织CSE mRNA水平。结果：钙化组大鼠心肌组织钙含量较对照组高3.8倍,主动脉钙含量、［45Ca2+］ 沉积及ALP 活性分别较对照组高6.8倍、1.4倍和 1.9倍（P＜0.01）；钙化组大鼠血浆H2S含量较对照组低39%（P<0.01），心肌和主动脉组织的 H2S含量也分别较对照组低39%和31%，CSE mRNA表达也分别低28％和36％（P<0.01），CSE活性分别低56%和53%(P<0.01)。结论：钙化心血管组织CSE/H2S通路受抑制，内源性H2S生成减少。

Down-regulation of glutamyl cysteine cystathionine-lyase/hydrogen sulfide system in rat cardiovascular calcification

AIM: To observe the changes of cystathionine-lyase/hydrogen sulfide(CSE/H_2S) in vivo in vascular calcification and to explore the role of CSE/H_2S in vascular calcification.METHODS: Vascular calcification model in rats was induced by administration of vitamin D_3 plus nicotine.The extent of calcification was estimated by assaying calcium content.~(45)Ca~(2 )] deposition and alkaline phosphatase(ALP) activity were detected.CSE mRNA amount was determined by using competitive quantitative RT-PCR.The content of H_2S and activity of CSE in the plasma and cardiovascular tissues were also determined with biochemical methods.RESULTS: Calcium content in myocardium increased by 3.8 folds in a calcification model.Compared to control,calcium content,~(45)Ca~(2 )] accumulation and ALP activity in calcified arteries increased by 6.8,1.4,and 1.9 folds,respectively(P<0.01).H_2S contents in plasma,myocardium and aorta were 39%,39% and 31% lower than those in control group(P<0.01).The gene expression of CSE was down-regulated in myocardium and aorta.Compared to control group,the amount of CSE mRNA in myocardium and calcified aorta were decreased by 28% and 36%,respectively(P<0.01).The activity of CSE was 56% and 53% lower than that in control(P<0.01).CONCLUSION: The production of H_2S,the gene expression and activity of CSE are down-regulated in the cardiovascular calcification,suggesting that the decrease in H_2S production plays a role in the pathogenesis of vascular calcification.