| 邢 燕,历 飞,林大勇,刘 鸿,白 剑.甘草次酸通过PI3K-AKT途径抑制H2O2所致大鼠心肌细胞氧化损伤[J].现代生物医学进展英文版,2018,(6):1044-1049. |
| 甘草次酸通过PI3K-AKT途径抑制H2O2所致大鼠心肌细胞氧化损伤 |
| Glycyrrhetinic Acid Decreases H2O2-induced Oxidative Injury of H9C2 Cells through PI3K-AKT Pathway |
| Received:September 30, 2017 Revised:November 02, 2017 |
| DOI：10.13241/j.cnki.pmb.2018.06.009 |
| 中文关键词: 甘草次酸 AKT途径 凋亡 活性氧 |
| 英文关键词: Glycyrrhetinic acid AKT pathway Apoptosis Reactive oxygen species |
| 基金项目:辽宁省自然科学基金项目（201618） |
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| 中文摘要: |
| 摘要 目的：研究甘草次酸对H2O2所致大鼠心肌细胞氧化损伤的影响及其可能机制。方法：采用H2O2处理建立H9c2大鼠心肌细胞氧化损伤模型后，比较模型中ROS生成和细胞凋亡比例，使用不同浓度的甘草次酸孵育H9c2细胞24、48h后，通过流式细胞仪检测ROS的生成量，Annexin V-FITC/ PI双标记流式细胞术检测凋亡率，蛋白质印迹法检测检PI3K、AKT1、p-AKT蛋白的表达。结果：H9c2大鼠心肌细胞氧化损伤模型中ROS生成和细胞凋亡率分别为(49.33±3.23)%和(33.89±1.45)%，与对照组相比有显著差异；100 μmol/L和200 μmol/L的甘草次酸作用24 h后，H9c2大鼠心肌细胞氧化损伤模型中表达ROS细胞的比例(35.39±1.24)%和(30.46±0.95)%，凋亡细胞比例分别为(29.47±3.15)%和(23.17±1.46)%，当作用48 h后，H9c2大鼠心肌细胞氧化损伤模型中表达ROS细胞的比例(42.67±1.89)%和(35.49±1.63）%，凋亡细胞比例分别为(40.22±3.06)%和(35.26±2.78)%，与对照组相比有显著性差异；使用渥曼青霉素后，各甘草次酸组的与对照组无显著性差异。结论：甘草次酸可能通过PI3K-AKT途径抑制H2O2所致大鼠心肌细胞氧化损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effect and mechanism of glycyrrhetinic acid on the oxidative injury of rat myocardial cells. Methods: Rat myocardial H9c2 cells were treated by H2O2 to induce oxidative injury. The ROS generation and apoptosis were detected. Different concentrations of glycyrrhetinic acid were used to treat H2O2-induced H9c2 cells for 24 h and 48 h. of the ROS generation in H9c2 cells was detected by flow cytometry; proportion of apoptotic cells was detected by flow cytometry with Annexin V/PI double marker staining; PI3K, AKT1, p-AKT protein expressions were detected by Western blotting. Results: The ROS generation and cell apoptotic rate in H2O2-induced H9c2 cells were (49.33±3.23)% and (33.89±1.45)% respectively, which were significantly higher than those of the control group. 100 μmol/L and 200 μmol/L glycyrrhetinic acid obviously decreased the ROS generation[(35.39±1.24)% and (30.46±0.95)%], ratios of apoptotic cell[(29.47±3.15)% and (23.17±1.46)%] in H9c2 cells treated by H2O2 for 24 hours; 100μmol/L and 200μmol/L glycyrrhetinic acid obviously decreased the ROS generation[(42.67±1.89)% and (35.49±1.63)%], ratios of apoptotic cells[(40.22±3.06)% and (35.26±2.78)%] in H9c2 cells treated by H2O2 for 48 hours; wortmannin showed similar effect with glycyrrhetinic acid. Conclusion: Glycyrrhetinic acid could decrease the generation of ROS and apoptosis in H2O2-induced oxidative injury of H9c2 cells through PI3K-AKT pathway. |
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