维生素D缺乏对小鼠心肌氧化应激水平的影响及机制研究
发布时间：2019-01-01 12:19
【摘要】：目的既往研究结果显示维生素D缺乏与心室重构的发生密切相关,但具体机制尚未明确。氧化应激增加在心室重构发生与进展过程中发挥重要的作用,文中拟探讨维生素D缺乏对小鼠心肌氧化应激水平的影响及可能相关的信号通路。方法实验采用3周龄的C57小鼠,随机数字表法分成3组:维生素D缺乏组(维生素D缺乏饲料喂养10周),维生素D充足组(维生素D充足饲料喂养10周)及维生素D缺乏后补充组(维生素D缺乏饲料喂养10周后,转为维生素D充足饲料喂养+骨化三醇治疗10周)。建模成功后,检测小鼠血液中25羟维生素D3水平及相关生化指标,心脏超声检查小鼠心脏腔室内径,8-OHDG染色测定小鼠心肌阳性细胞数,分别提取心肌线粒体蛋白、细胞核蛋白及总蛋白,Western blot检查TXNIP、ASK-1、P-ASK-1、细胞色素C等蛋白表达量。结果心脏超声结果显示维生素D充足组小鼠与维生素D缺乏组小鼠相比较,心肌的左室舒张末期直径及左室质量指数均显著增高[(3.820±0.125)mm vs(3.748±0.092)mm,(119.30±8.54)vs(97.60±3.65),P0.05)。在对小鼠心肌切片进行8-OHDG染色后发现,维生素D充足组小鼠心肌中8-OHDG染色阳性的心肌细胞数(65.4±2.3)显著高于维生素D缺乏组(21.8±1.6),而补充骨化三醇后,可使8-OHDG染色阳性的心肌细胞数明显回落(36.4±1.5)。Western blot检查结果提示,维生素D充足组小鼠心肌中TXNIP蛋白的表达显著上调,并伴随有P-ASK1/ASK-1的比值增加,Cyt C的释放及Cleaved caspase3的增加。结论维生素D缺乏可以引起心肌的氧化应激损伤,而损伤发生的机制可能与TXNIP蛋白表达的上调及ASK-1相关的细胞凋亡通路的激活有关。
[Abstract]:Objective previous studies have shown that vitamin D deficiency is closely related to ventricular remodeling, but the mechanism is not clear. The increase of oxidative stress plays an important role in the development and progression of ventricular remodeling. This paper aims to explore the effects of vitamin D deficiency on the level of oxidative stress in myocardium of mice and the related signaling pathways. Methods three week-old C57 mice were randomly divided into three groups: vitamin D deficiency group (fed with vitamin D deficiency for10 weeks). Vitamin D group (vitamin D sufficient feed feeding for 10 weeks) and vitamin D deficiency supplementation group (vitamin D deficiency feed feeding for 10 weeks, fed with vitamin D sufficient feed for 10 weeks to feed ossifying triol treatment for 10 weeks). After the establishment of the model, the levels of 25 hydroxyvitamin D _ 3 in blood and related biochemical indexes were detected, the heart cavity diameter was examined by echocardiography, the number of positive cells in myocardium was determined by 8-OHDG staining, and the myocardial mitochondrial protein was extracted, respectively. Nuclear protein and total protein, Western blot were used to detect the expression of TXNIP,ASK-1,P-ASK-1, cytochrome C and other proteins. Results the results of echocardiography showed that the left ventricular end-diastolic diameter and left ventricular mass index in the vitamin D group were significantly higher than those in the vitamin D deficiency group [(3.820 卤0.125) mm vs (3.748 卤0.092) mm,]. (119.30 卤8.54) vs (97.60 卤3.65, P0.05). After 8-OHDG staining in myocardial sections of mice, it was found that the number of myocardial cells positive for 8-OHDG staining in sufficient vitamin D group (65.4 卤2.3) was significantly higher than that in vitamin D deficient group (21.8 卤1.6). However, the number of myocardial cells positive for 8-OHDG staining was significantly decreased after supplementation of calcitriol (36.4 卤1.5). Western blot). The results showed that the expression of TXNIP protein was significantly up-regulated in the myocardium of mice with sufficient vitamin D. The ratio of P-ASK1/ASK-1 increased the release of, Cyt C and the increase of Cleaved caspase3. Conclusion Vitamin D deficiency can induce oxidative stress injury in myocardium, and the mechanism of injury may be related to the up-regulation of TXNIP protein expression and the activation of apoptosis pathway associated with ASK-1.
【作者单位】： 南京军区南京总医院心内科;
【基金】：南京军区总医院科研基金(2013048)
【分类号】：R591.44
本文编号：2397555
[Abstract]:Objective previous studies have shown that vitamin D deficiency is closely related to ventricular remodeling, but the mechanism is not clear. The increase of oxidative stress plays an important role in the development and progression of ventricular remodeling. This paper aims to explore the effects of vitamin D deficiency on the level of oxidative stress in myocardium of mice and the related signaling pathways. Methods three week-old C57 mice were randomly divided into three groups: vitamin D deficiency group (fed with vitamin D deficiency for10 weeks). Vitamin D group (vitamin D sufficient feed feeding for 10 weeks) and vitamin D deficiency supplementation group (vitamin D deficiency feed feeding for 10 weeks, fed with vitamin D sufficient feed for 10 weeks to feed ossifying triol treatment for 10 weeks). After the establishment of the model, the levels of 25 hydroxyvitamin D _ 3 in blood and related biochemical indexes were detected, the heart cavity diameter was examined by echocardiography, the number of positive cells in myocardium was determined by 8-OHDG staining, and the myocardial mitochondrial protein was extracted, respectively. Nuclear protein and total protein, Western blot were used to detect the expression of TXNIP,ASK-1,P-ASK-1, cytochrome C and other proteins. Results the results of echocardiography showed that the left ventricular end-diastolic diameter and left ventricular mass index in the vitamin D group were significantly higher than those in the vitamin D deficiency group [(3.820 卤0.125) mm vs (3.748 卤0.092) mm,]. (119.30 卤8.54) vs (97.60 卤3.65, P0.05). After 8-OHDG staining in myocardial sections of mice, it was found that the number of myocardial cells positive for 8-OHDG staining in sufficient vitamin D group (65.4 卤2.3) was significantly higher than that in vitamin D deficient group (21.8 卤1.6). However, the number of myocardial cells positive for 8-OHDG staining was significantly decreased after supplementation of calcitriol (36.4 卤1.5). Western blot). The results showed that the expression of TXNIP protein was significantly up-regulated in the myocardium of mice with sufficient vitamin D. The ratio of P-ASK1/ASK-1 increased the release of, Cyt C and the increase of Cleaved caspase3. Conclusion Vitamin D deficiency can induce oxidative stress injury in myocardium, and the mechanism of injury may be related to the up-regulation of TXNIP protein expression and the activation of apoptosis pathway associated with ASK-1.
【作者单位】： 南京军区南京总医院心内科;
【基金】：南京军区总医院科研基金(2013048)
【分类号】：R591.44
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