| 赵志林,白 锋,任旭爱,丁邵祥,伏晓琳,尹志勇.Trx通过Sirt3-P53通路促进自噬并改善高糖诱发的CMECs损伤[J].现代生物医学进展英文版,2017,17(29):5642-5645. |
| Trx通过Sirt3-P53通路促进自噬并改善高糖诱发的CMECs损伤 |
| Thioredoxin Increase the Autophagy to Alleviate Cardiac Microvascular Endothelial Cells Injury Induced by High Glucose via Sirt3-P53 Pathway |
| Received:December 30, 2016 Revised:January 26, 2017 |
| DOI：10.13241/j.cnki.pmb.2017.29.009 |
| 中文关键词: 硫氧还蛋白 自噬 心脏微血管内皮细胞 糖尿病 |
| 英文关键词: Thioredoxin Autophagy Cardiac microvascular endothelial cell Diabetes |
| 基金项目: |
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| 中文摘要: |
| 摘要 目的：明确硫氧还蛋白（Thioredoxin, Trx）通过自噬调节对大鼠心脏微血管内皮细胞损伤的保护作用及相关机制。方法：分离成年大鼠心脏微血管内皮细胞并分为：①正常对照组；②高糖组；③高糖+Trx组；④高糖+ Trx+ Ad-shSirt3组；⑤高糖+ Trx+ Ad-shP53组；⑥高糖+ DMSO空载组。通过In Vitro Vascular Permeability Assay Kit检测单层心脏微血管内皮细胞通透性，TUNEL染色检测细胞凋亡，Western blot法检测Sirt3、P53、Atg5、LC3BI/II等相关自噬相关信号通路关键蛋白的表达水平。结果：与正常对照组相比，高糖引起单层心脏微血管内皮细胞通透功能损伤，增加细胞凋亡，抑制自噬，且Sirt3、Atg5、LC3BI/II表达下降而P53表达上升；给予Trx可以上调Sirt3、Atg5、LC3BI/II蛋白表达水平，抑制P53表达，并显著减轻上述高糖引起的细胞损伤；但是，分别干扰Sirt3和P53表达后，Trx的作用明显减弱。结论：Trx通过Sirt3-P53信号通路促进心脏微血管内皮细胞自噬，降低细胞凋亡，改善高糖诱发的大鼠心脏微血管内皮细胞损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the protective role and Sirt3-P53 related mechanism of Thioredoxin in rat cardiac microvas- cular endothelial cells injury induced by high glucose. Methods: Adult rat cardiac microvascular endothelial cells (CMECs) were cultured and divided to six groups including: ① Control Group; ② High-Glucose Group; ③ HG+Trx Group; ④ HG+Trx+ Ad-shSirt3 Group; ⑤ HG+Trx+ Ad-shP53 Group; ⑥ HG+Vehicle Group. Permeability of monolayer CMECs was tested by In Vitro Vascular Permeability As- say Kit; Cellular apoptosis was detected by TUNEL staining; And Western Blot was used to analyze the protein expression including Sirt3, P53, Atg5 and LC3BI/II. Results: Compared with Control Group, the Permeability of monolayer CMECs and cellular apoptosis were increased by high glucose, which also reduced autophagy. The expression of Sirt3, Atg5 and LC3BI/II were on the decline and the P53 on rise. Trx could alleviate CMECs permeability injury as well as apoptosis and promoted cellular autophagy. At meaning while, Sirt3, Atg5 and LC3BI/II expression were increased and P53 expression were decreased by Trx. In addition, while Sirt3 or P53 were knockdown by siRNA, the protective role of Trx was interfered obviously. Conclusion: Trx can enhance CMECs autophagy and attenu- ate apoptosis through Sirt3-P53 pathway, which is helpful to alleviate injury induced by high glucose. |
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