Magnesium prevents β-glycerophosphate-induced calcification in rat aortic vascular smooth muscle cells
Magnesium prevents β-glycerophosphate-induced calcification in rat aortic vascular smooth muscle cells
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DOI：
10.3892/br.2015.473
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发表时间：
2015-07-01
影响因子：
2.3
通讯作者：
Feng, Xunwei
中科院分区：
文献类型：
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作者：
Bai, Yaling;Zhang, Junxia;Feng, Xunwei
血管钙化（VC）是慢性肾脏病患者的一个主要问题，其中高血磷起着关键作用。临床研究表明，镁对VC有保护作用。然而，关于高血清镁对VC在细胞水平上的影响的研究很少，需要进一步调查。因此，本研究探讨镁对β-甘油磷酸盐（BGP）诱导的大鼠主动脉血管平滑肌细胞（RAVSMCs）钙化的影响。在本研究中，镁的加入减少了钙沉积，而BGP增加了钙沉积。较高的镁水平抑制BGP诱导的碱性磷酸酶（ALP）活性，并降低核心结合因子α-1（Cbf α 1）的表达。总之，较高的镁水平可防止BGP诱导的RAVSMC钙化，并抑制Cbf α 1和ALP的表达。因此，镁正在影响与VC相关的Cbf α 1和ALP的表达，并且可能在临床情况下对VC发挥作用。
Vascular calcification (VC), in which high serum phosphate plays a critical role, is one major problem in patients with chronic kidney disease. Clinical studies report that magnesium has a protective effect on VC. However, the studies regarding the impact of high serum magnesium on VC at a cellular level are few and require further investigation. Therefore, the present study explored the effect of magnesium on calcification induced by beta-glycerophosphate (BGP) in rat aortic vascular smooth muscle cells (RAVSMCs). In the present study, the addition of magnesium decreased calcium deposition, which was increased by BGP. Higher magnesium levels inhibited BGP-induced alkaline phosphatase (ALP) activity and decreased the expression of core-binding factor alpha-1 (Cbf alpha 1). In conclusion, higher magnesium levels prevented BGP-induced calcification in RAVSMCs and inhibited the expression of Cbf alpha 1 and ALP. Thus, magnesium is influencing the expression of Cbf alpha 1 and ALP associated with VC and may have the potential to serve as a role for VC in clinical situations.