线粒体MnSOD对MnSOD-Tg小鼠钙化模型的血管ALP活性和转录因子表达的影响  被引量:1

Influence of mitochondrial MnSOD on vascular ALP activity and transcription factor expressions in mice model of vascular calcification

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作  者:许耘红[1] 何穗镕 李丽青[1] 刘婉婷[2] 

机构地区:[1]广州医科大学附属第三医院心内科,广东广州510150 [2]广州医科大学附属第三医院神经内科,广东广州510150

出  处:《心血管康复医学杂志》2016年第1期35-37,共3页Chinese Journal of Cardiovascular Rehabilitation Medicine

摘  要:目的:观察线粒体锰超氧化物歧化酶(MnSOD)对MnSOD-Tg小鼠钙化模型的血管碱性磷酸酶(ALP)活性、转录因子:Runx2和成骨细胞特异性转录因子Osterix表达水平的影响。方法:选取野生型(WT)、MnSOD-Tg小鼠各20只,分别作为WT组和MnSOD-Tg组,并建立小鼠血管钙化模型。比较分析两种小鼠血管ALP活性、Runx2和转录因子Osterix表达水平之间的差异。结果:造模成功后,与WT组比较,MnSOD-Tg组ALP活性[(75.89±4.17)比(61.32±3.12)]、Runx2[(0.928±0.016)比(0.694±0.007)]和转录因子Osterix表达水平[(0.472±0.036)比(0.257±0.013)]均显著降低,P均<0.01。结论:锰超氧化物歧化酶可能通过降低血管碱性磷酸酶活性、Runx2和转录因子Osterix的表达水平,起到改善动脉粥样硬化的作用。Objective: To observe influence of mitochondrial manganese superoxide dismutase (MnSOD) on vascular alkaline phosphatase (ALP) activity, transcription factor: Runx2 and Osterix expression levels in MnSOD-Tg mice model of vascular calcification. Methods: A total of 20 wild type (WT) mice were selected as WT group and 20 Mn- SOD-Tg mice were enrolled as MnSOD-Tg group, then mice model of vascular calcification was established. Vascu- lar ALP activity, expression levels of transcription factor Runx2 and Osterix were compared and analyzed between two groups. Results.. After successful niodel establishment, compared with WT group, there were significant reduc- tions in ALP activity [ (75.89 ± 4. 17) vs. (61.32 ± 3.12)], expression levels of transcription factor Runx2 [ (0. 928±0. 016) vs. (0. 694 ± 0. 007)] and Osterix [ (0. 472 ± 0. 036) vs. (0. 257 ± 0. 013)] in MnSOD-Tg group, P〈0.01 all. Conclusion: Manganese superoxide dismutase may be improving atherosclerosis via reducing activity of vascular alkaline phosphatase, expression levels of transcription factor Runx2 and Osterix.

关 键 词:超氧化物歧化酶 碱性磷酸酶 血管钙化 

分 类 号:R543.509[医药卫生—心血管疾病]

 

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