| 沈红枫,夏海江,刘龙斌.人参皂苷Re通过miR-221-3p/ESR1/SLC7A11减轻缺氧/复氧心肌细胞损伤的机制研究[J].浙江中西医结合杂志,2026,36(5): |
| 人参皂苷Re通过miR-221-3p/ESR1/SLC7A11减轻缺氧/复氧心肌细胞损伤的机制研究 |
| Study on the Mechanism of Ginsenoside Re in Alleviating Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury via miR-221-3p/ESR1/SLC7A1 |
| 投稿时间：2025-07-17 修订日期：2026-04-04 |
| DOI： |
| 中文关键词: 人参皂苷Re、缺氧/复氧心肌损伤、雌激素受体1、miR-221-3p |
| 英文关键词:Ginsenoside Re, Hypoxia/reoxygenation-induced myocardial injury, Estrogen receptor 1, miR-221-3p |
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| 中文摘要: |
| 目的 观察人参皂苷Re对缺氧/复氧（hypoxia-reoxygenation，H/R）心肌细胞活性及微小RNA-221-3p（microRNA-221-3p，miR-221-3p）/雌激素受体1（Estrogen receptor 1，ESR1）/溶质载体家族7成员11（Solute carrier family 7 member 11，SLC7A11）通路的影响。方法 将H9C2细胞缺氧培养12 h再复氧培养12 h构建制备H/R 细胞模型，并采用50 μmol/L人参皂苷Re干预，通过细胞计数试剂盒-8（Cell Counting Kit-8，CCK-8）观察细胞活性，通过定量实时聚合酶链式反应（Quantitative real-time polymerase chain reaction，qRT-PCR）实验检测miR-221-3p表达，通过免疫蛋白印迹实验对比各组ESR1、SLC7A11蛋白表达水平，通过活性氧检测试剂盒检测活性氧水平，通过酶联免疫吸附实验检测谷胱甘肽（Glutathione，GSH）、4-羟基壬烯醛（4-hydroxynonenal,4-HNE）、细胞上清乳酸脱氢酶（lactate dehydrogenase,LDH）表达水平，通过比色法对比丙二醛（Malondialdehyde，MDA）水平。结果 与对照组相比，H/R H9C2细胞存活率下降（100.00±7.00% VS 55.05±4.33%，P<0.001），miR-221-3p（1.00±0.00 VS 0.33±0.05，P=0.02）、4-NHE（634.41±31.50pg/ml VS 960.85±12.41pg/ml，P<0.001）、活性氧水平（100.00±3.79% VS 217.60±8.27%，P<0.001）、细胞上清LDH（5.47±0.14ng/ml VS 8.93±0.29ng/ml，P<0.001）、MDA（6.56±0.83 VS 20.36±0.85μmol/L，P<0.001）升高，ESR1（1.00±0.00 VS 0.79±0.07，P=0.035）、SLC7A11（1.00±0.00 VS 0.73±0.12，P=0.01）、GSH（17.79±0.44μg/ml VS 14.26±0.48μg/ml，P<0.001）蛋白表达下降；人参皂苷Re能够提高H/R H9C2细胞存活率（55.05±4.33% VS 82.14±2.27%，P<0.001），降低miR-221-3p（0.33±0.05 VS 2.71±0.85，P=0.02）、4-NHE（960.85±12.41pg/ml VS 812.67±10.58pg/ml ，P<0.001）、活性氧（217.60±8.27% VS 137.32±26.04%，P<0.001）、细胞上清LDH（8.93±0.29ng/ml VS 6.91±0.33ng/ml，P<0.001）、MDA（20.36±0.85μmol/L VS 11.07±0.74μmol/L，P<0.001）水平，并升高ESR1（0.79±0.07 VS 1.11±0.14，P=0.008）、SLC7A11（0.73±0.12 VS 0.96±0.09，P=0.02）、GSH（14.26±0.48μg/ml VS 16.19±0.26μg/ml，P=0.001）蛋白表达。结论 人参皂苷Re能够改善心肌细胞H/R损伤，其机制可能与调控miR-221-3p/ESR1/SLC7A11通路相关。 |
| 英文摘要: |
| Objective This study aims to investigate the effects of ginsenoside Re on hypoxia/reoxygenation (H/R)-induced injury in H9C2 cardiomyocytes, with a focus on its potential regulatory role in the miR-221-3p/ESR1/SLC7A11 signaling pathway. Methods An in vitro H/R cell model was established by subjecting H9C2 cardiomyocytes to 12 hours of hypoxia followed by 12 hours of reoxygenation. Ginsenoside Re (50 μmol/L) was administered as treatment. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8). The expression level of miR-221-3p was quantified via quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression levels of estrogen receptor 1 (ESR1) and solute carrier family 7 member 11 (SLC7A11) were evaluated by Western blotting. Intracellular reactive oxygen species (ROS) levels were measured using reactive oxygen species assay kit., while concentrations of lactate dehydrogenase (LDH) in cell supernatant， glutathione (GSH), and 4-hydroxynonenal (4-HNE) were determined via enzyme-linked immunosorbent assay (ELISA). The level of malondialdehyde (MDA) was compared by colorimetry. Results Compared with the control group, H/R-treated H9C2 cells exhibited a significantly decreased cell viability (100.00 ± 7.00% vs. 55.05 ± 4.33%, P < 0.001), accompanied by upregulation of miR-221-3p (1.00 ± 0.00 vs. 0.33 ± 0.05, P = 0.02), increased levels of 4-HNE (634.41 ± 31.50 pg/mL vs. 960.85 ± 12.41 pg/mL, P < 0.001), reactive oxygen species (100.00 ± 3.79% vs. 217.60 ± 8.27%, P < 0.001), lactate dehydrogenase (LDH) in the cell supernatant (5.47 ± 0.14 ng/mL vs. 8.93 ± 0.29 ng/mL, P < 0.001), and malondialdehyde (MDA) (6.56 ± 0.83 vs. 20.36 ± 0.85 μmol/L, P < 0.001). In addition, protein expression levels of ESR1 (1.00 ± 0.00 vs. 0.79 ± 0.07, P = 0.035), SLC7A11 (1.00 ± 0.00 vs. 0.73 ± 0.12, P = 0.01), and glutathione (GSH) (17.79 ± 0.44 μg/mL vs. 14.26 ± 0.48 μg/mL, P < 0.001) were significantly downregulated. Treatment with ginsenoside Re markedly improved cell viability in H/R-injured H9C2 cells (55.05 ± 4.33% vs. 82.14 ± 2.27%, P < 0.001), reduced the expression of miR-221-3p (0.33 ± 0.05 vs. 2.71 ± 0.85, P = 0.02), and attenuated the elevation of 4-HNE (960.85 ± 12.41 pg/mL vs. 812.67 ± 10.58 pg/mL, P < 0.001), reactive oxygen species (217.60 ± 8.27% vs. 137.32 ± 26.04%, P < 0.001), LDH release (8.93 ± 0.29 ng/mL vs. 6.91 ± 0.33 ng/mL, P < 0.001), and MDA levels (20.36 ± 0.85 μmol/L vs. 11.07 ± 0.74 μmol/L, P < 0.001). Furthermore, ginsenoside Re restored the protein expression of ESR1 (0.79 ± 0.07 vs. 1.11 ± 0.14, P = 0.008), SLC7A11 (0.73 ± 0.12 vs. 0.96 ± 0.09, P = 0.02), and GSH (14.26 ± 0.48 μg/mL vs. 16.19 ± 0.26 μg/mL, P = 0.001).. Conclusion Ginsenoside Re demonstrates protective effects against H/R-induced injury in H9C2 cardiomyocytes, potentially through modulation of the miR-221-3p/ESR1/SLC7A11 pathway. |
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