[1]蒋丽,芮燕君,戴佳琪,等.丹参酮IIA对过氧化氢诱导的人晶状体上皮细胞凋亡和氧化应激的影响[J].眼科新进展,2021,41(9):838-842.[doi:10.13389/j.cnki.rao.2021.0175]
　JIANG Li,RUI Yanjun,DAI Jiaqi,et al.Influence of tanshinone IIA on H2O2-induced apoptosis and oxidative stress in human lens epithelial cells via activating the Nrf2/HO-1 pathway[J].Recent Advances in Ophthalmology,2021,41(9):838-842.[doi:10.13389/j.cnki.rao.2021.0175]
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丹参酮IIA对过氧化氢诱导的人晶状体上皮细胞凋亡和氧化应激的影响/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
41卷
期数:
2021年9期
页码:
838-842
栏目:
实验研究
出版日期:
2021-09-05

文章信息/Info

Title:
Influence of tanshinone IIA on H2O2-induced apoptosis and oxidative stress in human lens epithelial cells via activating the Nrf2/HO-1 pathway
作者:
蒋丽; 芮燕君; 戴佳琪; 丁高凤
200000　上海市，中南大学附属爱尔眼科医院
Author(s):
JIANG Li; RUI Yanjun; DAI Jiaqi; DING Gaofeng
Aier Eye Hospital Affiliated to Central South University，Shanghai 200000,China
关键词:
丹参酮IIA; 氧化应激; 细胞凋亡; 人晶状体上皮细胞; 核因子E2相关因子2; 血红素氧合酶-1
Keywords:
tanshinone IIA;  oxidative stress;  apoptosis;  human lens epithelial cells;  Nrf2;  heme oxygenase-1
分类号:
R776
DOI:
10.13389/j.cnki.rao.2021.0175
文献标志码:
A
摘要:
目的　探讨丹参酮IIA（Tan IIA）对过氧化氢（H2O2）诱导的人晶状体上皮细胞凋亡和氧化应激的调控作用及可能的机制。方法　以人晶状体上皮细胞SRA01/04为研究对象，分为空白组、H2O2组（H2O2处理细胞建立氧化损伤模型）、Tan IIA组（Tan IIA溶液预处理24 h后，H2O2作用24 h）、Tan IIA+siNC组（转染阴性对照，其他处理方式同Tan IIA组）和Tan IIA+siNrf2组［转染核因子E2相关因子2（Nrf2） siRNA(siNrf2)，其他处理方式同Tan IIA组］。CCK-8法检测细胞活力，流式细胞术分别检测细胞凋亡率和活性氧簇（ROS）水平，酶联免疫吸附试验测定细胞中过氧化氢酶（CAT）活性、超氧化物歧化酶（SOD）含量、谷胱甘肽过氧化物酶（GSH-Px）含量，Western blot检测细胞总蛋白中Nrf2、血红素氧合酶-1（HO-1）表达及核蛋白中Nrf2表达情况。结果　通过CCK-8法确定H2O2和Tan IIA最佳实验浓度为300 μmol·L-1和20 μmol·L-1。与空白组相比，H2O2组SRA01/04细胞活力及细胞中CAT活性、SOD含量、GSH-Px含量均降低，凋亡率和ROS水平均增加，同时总蛋白中Nrf2和HO-1蛋白相对表达量及核蛋白中Nrf2蛋白相对表达量均下调（均为P<0.05）。与H2O2组相比，Tan IIA组SRA01/04细胞活力及细胞中CAT活性、SOD含量、GSH-Px含量均增加，凋亡率和ROS水平均降低，总蛋白中Nrf2和HO-1蛋白相对表达量及核蛋白中Nrf2蛋白相对表达量均上调（均为P<0.05）。而沉默Nrf2基因后，Tan IIA对SRA01/04细胞的保护作用被逆转。结论　Tan IIA能够抑制H2O2诱导的人晶状体上皮细胞氧化应激性损伤和凋亡，其机制与Nrf2/HO-1通路的激活有关。
Abstract:
Objective　To study the effect of tanshinone IIA (Tan IIA) on H2O2-induced apoptosis and oxidative stress in human lens epithelial cells, and the possible mechanism.Methods　The human lens epithelial cell line SRA01/04 was divided into blank group, H2O2 group (treated with H2O2), Tan IIA group (pre-treated with 300 μmol·L-1 Tan IIA solution for 24 h before H2O2 exposure for 24 h), Tan IIA+siNC group (pre-treated with 300 μmol·L-1 Tan IIA solution for 24 h before H2O2 exposure for 24 h in cells transfected with siNC) and Tan IIA + siNrf2 group (pre-treated with 300 μmol·L-1 Tan IIA solution for 24 h before H2O2 exposure for 24 h in cells transfected with siNrf2). The cell viability was measured by CCK-8 assay. The apoptosis rate and the reactive oxygen species (ROS) level were measured by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was used to detect the activity of catalase (CAT) and the contents of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Western blot was used to detect protein levels of Nrf2 and heme oxygenase-1 (HO-1).Results　The optimal concentrations of H2O2 and Tan IIA solution were determined by CCK-8 assay at 300 μmol·L-1 and 20 μmol·L-1, respectively. Compared with the blank group, the cell viability, CAT activity, and SOD and GSH-Px contents decreased, while the apoptosis rate and ROS level increased in SRA01/04 cells of H2O2 group. Moreover, expression levels of total Nrf2 and HO-1, and nuclear protein level of Nrf2 were down-regulated (all P<0.05). Compared with H2O2 group, the viability, CAT activity, and SOD and GSH-Px contents increased, while the apoptosis rate and ROS level decreased in SRA01/04 cells of Tan IIA group. Meanwhile, protein levels of total Nrf2 and HO-1, and nuclear protein level of Nrf2 were up-regulated (all P<0.05). The protective effect of Tan IIA on SRA01/04 cells was reversed by silencing Nrf2.Conclusion　Tanshinone IIA can inhibit H2O2-induced apoptosis and oxidative stress in human lens epithelial cells via activating the Nrf2/HO-1 pathway.

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更新日期/Last Update: 2021-09-05