[1]韩学超,徐菁蔓,徐森,等.线粒体通透性转换孔在天麻素抗心肌细胞氧化应激损伤中的作用[J].南方医科大学学报,2018,(11):1306.[doi:10.12122/j.issn.1673-4254.2018.11.05]
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线粒体通透性转换孔在天麻素抗心肌细胞氧化应激损伤中的作用()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2018年11期
页码:
1306
栏目:
出版日期:
2018-11-30

文章信息/Info

Title:
Role of mitochondrial permeability transition pore in mediating the inhibitory effect of gastrodin on oxidative stress in cardiac myocytes in vitro
作者:
韩学超徐菁蔓徐森孙雅涵何玛莉李晓东李心雨皮佳仪于睿田炜
关键词:
氧化应激损伤线粒体通透性转换孔天麻素环孢菌素A
Keywords:
oxidative stress injury mitochondrial permeability transition pore gastrodin cyclosporin
DOI:
10.12122/j.issn.1673-4254.2018.11.05
摘要:
目的探讨H9c2心肌细胞发生氧化应激损伤时,线粒体膜上的线粒体通透性转换孔(mPTP)在天麻素抗氧化应激损伤的 保护机制中所发挥的作用。方法本实验分为6组:正常组,过氧化氢组,天麻素+过氧化氢组,天麻素组,环孢菌素A组,环孢菌 素A+天麻素+过氧化氢组。通过加入环孢菌素A(mPTP开放剂)观察天麻素的保护作用是否被抑制。用MTT法初步检测各组 细胞存活率,采用Annexin V-FITC/PI双染法通过流式细胞仪观察细胞早期凋亡率,大鼠三磷酸腺苷(ATP)试剂盒检测ATP的 含量,活性氧检测试剂盒检测细胞内活性氧(ROS)的含量,激光扫描共聚焦显微镜观察Jc-1标记的线粒体膜电位,Western blot 检测细胞内细胞色素C(Cyt C)含量,Caspase-3活性检测试剂盒检测caspase-3的酶活性。结果环孢菌素A+天麻素+过氧化氢 组线粒体的相对膜电位低于天麻素+过氧化氢组(1.98±0.18 vs 3.08±0.14),差异有统计学意义(P=0.014)。环孢菌素A可以阻断 氧化应激时天麻素降低细胞内活性氧和相关凋亡因子的含量、抑制相关因子活性的作用(P<0.05),并且在一定程度上阻断了天 麻素的抗凋亡作用(5.77±0.75)% vs(1.97±0.82)%,两者差异有统计学意义(P<0.001)。结论天麻素可以通过抑制心肌细胞发 生氧化应激损伤时mPTP的开放,最终通过减少凋亡来发挥一定的抗氧化应激损伤的作用。
Abstract:
Objective To explore the role of mitochondrial permeability transition pore (mPTP) in mediating the protective effect of gastrodin against oxidative stress damage in H9c2 cardiac myocytes. Methods H9c2 cardiac myocytes were treated with H2O2, gastrodin, gastrodin+H2O2, cyclosporin A (CsA), or CsA+gas+H2O2 group. MTT assay was used to detect the survival ratio of H9c2 cells, and flow cytometry with Annexin V-FITC/PI double staining was used to analyze the early apoptosis rate after the treatments. The concentration of ATP and level of reactive oxygen species (ROS) in the cells were detected using commercial kits. The mitochondrial membrane potential of the cells was detected with laser confocal microscopy. The expression of cytochrome C was detected with Western blotting, and the activity of caspase-3 was also assessed in the cells. Results Gastrodin pretreatment could prevent oxidative stress-induced reduction of mitochondrial membrane potential, and this effect was inhibited by the application of CsA. Gastrodin significantly lowered the levels of ROS and apoptosis-related factors in H2O2-exposed cells, and such effects were reversed by CsA. CsA significantly antagonized the protective effect of gastrodin against apoptosis in H2O2-exposed cells. Conclusions Gastrodin prevents oxidative stress-induced injury in H9c2 cells by inhibiting mPTP opening to reduce the cell apoptosis.

相似文献/References:

[1]黄艳平,杨天华,金植炎,等.线粒体通透性转换孔在内吗啡肽-1后处理减轻大鼠心肌缺血再灌注损伤中的作用[J].南方医科大学学报,2018,(05):547.

更新日期/Last Update: 1900-01-01