| 齐 晶,秦 毅,李兴培,冷 静,钟晓兰.丹参酮治疗冠心病对Nrf2/ARE信号通路和氧化应激的影响[J].,2024,(11):2015-2019 |
| 丹参酮治疗冠心病对Nrf2/ARE信号通路和氧化应激的影响 |
| The Effect of Nrf2/ARE Signaling Pathway and Oxidative Stress in Coronary Heart Disease Treated by Tanshinone |
| 投稿时间：2023-11-21 修订日期：2023-12-17 |
| DOI：10.13241/j.cnki.pmb.2024.11.003 |
| 中文关键词: 冠心病 丹参酮 核因子E2相关因子2 抗氧化反应元件 信号通路 氧化应激 心肌损伤 缺氧诱导因子-1α 凋亡 炎症 |
| 英文关键词: Coronary heart disease Tanshinone Nuclear factor E2 related factor 2 Antioxidant response element Signal pathway Oxidative stress Myocardial injury Hypoxia inducible factor-1α Apoptosis Inflammation |
| 基金项目:新疆维吾尔自治区自然科学基金项目（2022D01C269） |
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| 中文摘要: |
| 摘要 目的：分析丹参酮通过核因子E2相关因子2（Nrf2）/抗氧化反应元件（ARE）信号通路发挥抑制冠心病患者的氧化应激和心肌损伤的作用。方法：前瞻性纳入2022年6月至2023年6月我院诊断不稳定心绞痛患者84例为研究对象，随机分为对照组和观察组，每组各42例，对照组采用常规药物和介入干预，观察组加用丹参酮ⅡA磺酸钠注射液（剂量40 mg/d），连续治疗2周。比较两组治疗前后外周血Nrf2、ARE、缺氧诱导因子-1α（HIF-1α）和Caspase-1蛋白表达量，氧化应激指标活性氧簇（ROS）、丙二醛（MDA）和超氧化物歧化酶（SOD），炎症介质肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β，心肌损伤指标肌钙蛋白I（cTnI）和肌酸激酶同工酶（CK-MB）。结果：两组治疗前上述指标均无明显差异（P＞0.05），治疗后与治疗前比较改善明显（P＜0.05），且观察组Nrf2和ARE蛋白表达量显著高于对照组，而HIF-1α和Caspase-1蛋白表达量显著低于对照组，ROS水平下降，MDA和SOD水平升高，TNF-α和IL-1β降低，cTnI和CK-MB水平下降（P＜0.05）。结论：丹参酮可能通过激活Nrf2/ ARE信号通路发挥抑制冠心病患者的氧化应激、炎症反应、细胞凋亡以及心肌损伤的作用。 |
| 英文摘要: |
| ABSTRACT Objective: To analyze the effect of tanshinone inhibiting oxidative stress and myocardial injury in patients with coronary heart disease through nuclear factor E2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway. Methods: A prospective study was conducted on 84 patients with unstable angina pectoris diagnosis in our hospital from June 2022 to June 2023. They were randomly divided into control group and observation group, with 42 patients in each group. The control group received conventional drugs and intervention, while the observation group received tanshinone IIA sulfonate sodium injection (40 mg/d) on the basis of control group for 2 weeks continuous treatment. Comparisons of peripheral blood Nrf2, ARE, and hypoxia inducible factor-1α(HIF-1α) and Caspase-1 proteins expression, oxidative stress indicators such as reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD), inflammatory mediators tumor necrosis factor (TNF)-α and interleukin (IL)-1β, myocardial injury indicators troponin I (cTnI) and creatine kinase isoenzyme (CK-MB) were made between two groups before and after treatment. Results: There were no differences of above indicators between the two groups before treatment (P>0.05). After treatment, there were significant improvements compared to before treatment (P<0.05), and the expressions of Nrf2 and ARE proteins in observation group were significantly higher than those in control group, while HIF-1α and Caspase-1 proteins expression were significantly lower than control group, ROS level was less, MDA and SOD levels were higher, TNF-α and IL-1β levels were less, cTnI and CK-MB levels were lower, too(P<0.05). Conclusion: Tanshinone may inhibit oxidative stress, inflammatory response, cell apoptosis, and myocardial injury in patients with coronary heart disease by activating Nrf2/ARE signaling pathway. |
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