| 李雪连 关会林 王璐 郭瑞 赵丹丹 郭振丰 张佳琳 单宏丽.丹参酮IIA调节microRNA-1 保护缺氧心肌细胞的作用研究[J].,2014,14(28):5463-5467 |
| 丹参酮IIA调节microRNA-1 保护缺氧心肌细胞的作用研究 |
| Tanshinone IIA Protect Hypoxic Myocardial Cells ThroughRegulating MicroRNA-1 |
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| DOI： |
| 中文关键词: 丹参酮IIA 缺氧 心肌细胞 miR-1 细胞内钙 细胞凋亡 |
| 英文关键词: shinone II A Hypoxia Cardiomyocytes miRNA-1 [Ca2+]i Apoptosis |
| 基金项目:黑龙江省教育厅科学技术研究面上项目（12521176） |
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| 中文摘要: |
| 目的：研究丹参酮II A（TanshinoneIIA）通过调节microRNA-1 抗心肌细胞缺氧损伤的作用。方法：原代培养新生大鼠心肌细
胞，建立心肌细胞缺氧模型。MTT 法检测心肌细胞存活率(%)；TUNEL、流式细胞术测心肌细胞凋亡率；激光共聚焦检测心肌细胞
内钙离子[Ca2+]i 浓度的变化情况。结果：MTT 结果显示丹参酮IIA 对缺氧心肌细胞及过表达miR-1 引起心肌细胞损伤具有保护
作用。丹参酮IIA 增加了缺氧心肌细胞的存活率（P<0.05），同时给予丹参酮IIA 和miR-1 组与单独miR-1 损伤组相比较，存活率
也明显升高，呈现剂量依赖性。TUNEL结果显示丹参酮IIA 可以抑制缺氧诱导的细胞凋亡，丹参酮IIA 可以明显降低由缺氧导致
的细胞凋亡率（P<0.05）。共聚焦检测结果显示，缺氧损伤的心肌细胞内[Ca2+]i 显著升高1322.72± 5.16（vs正常对照组，P<0.05），
丹参酮IIA 则有效抑制由缺氧引起过高的[Ca2+]i。miR-1 诱导的细胞内[Ca2+]i 升高至1349.33± 62.63，约为正常对照组的1.96倍，
而丹参酮IIA 则有效抑制胞内过高的[Ca2+]i，从而发挥心肌保护作用。结论：丹参酮IIA可能是通过抑制胞内miR-1 的表达，参与
对钙离子浓度的调控，发挥其对心肌细胞的保护作用。 |
| 英文摘要: |
| Objective:To study and explore the mechanism of Tanshinone IIA (Tan) protecting hypoxic myocardial cells by
regulating microRNA-1.Methods:Primary cultured neonatal cardiomyocytes and established the model of myocardial hypoxia. Cell
viability was detected by MTT assay, apoptosis of myocardial cells and apoptosis percentage were detected by TUNEL assay and flow
cytometry. Intracellular calciumconcentration ([Ca2+]i) was measured by Laser Scanning Confocal.Results:MTT results showed that the
Tan IIA could alleviate cell death induced by hypoxia, with the trend of dose-dependence, (P<0.05). TUNEL results also showed that Tan
IIA could significantly reduce the percentage of hypoxia-induced apoptosis (P<0.05). The [Ca2+]i increased significantly under hypoxia,
while the Tan IIA could effectively inhibit the [Ca2+]i and thus play a protective role (P<0.05).Conclusion:Tanshinone IIA can alleviate
the hypoxia-induced apoptosis, possibly through regulating miRNA-1 and [Ca2+]i, playing a protective effect on myocardial cells. |
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