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氧化应激与再狭窄的相关性:一项病例对照研究。

Association between Oxidative Burden and Restenosis: A Case-Control Study.

机构信息

Department of Medical Biotechnology and Nanotechnology, Mashhad University of Medical Sciences, Mashhad, Iran.

Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

Oxid Med Cell Longev. 2022 Jun 28;2022:3577761. doi: 10.1155/2022/3577761. eCollection 2022.

DOI:10.1155/2022/3577761
PMID:35799893
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9256427/
Abstract

BACKGROUND

In-stent restenosis (ISR) is an important clinical complication that occurs following stent implantation. The application of drug-eluting stents (DES) and even consumption of drugs such as antiplatelet agents and statins are not completely effective in reducing ISR risk. Since the number of these patients continues to rise, it is pivotal to detect patients who are at a higher risk of ISR. In addition, identification of biochemical markers of ISR could give the right perspective on choosing the proper strategy to treat these patients. Several pathophysiological pathways including oxidative stress (OS) are implicated in the progression of ISR. Hence, this study aimed to evaluate the association between oxidative/anti-oxidative markers and ISR.

METHODS

This was a case-control study which comprised 21 ISR, 26 NISR (non-ISR), and 20 healthy subjects. The serum levels of OS markers including malondialdehyde (MDA), thiol groups (GSH), total antioxidant capacity (TAC), and the activity of serum antioxidant enzymes such as glutathione peroxidase (GPx) and superoxide dismutase (SOD) were assessed by colorimetric methods. The overall oxidative burden was assessed using a pro-oxidant-antioxidant balance (PAB) assay.

RESULTS

MDA levels were considerably higher in the ISR group when compared to healthy subjects ( = 0.004). PAB also indicated significantly higher values in both ISR ( < 0.001) and NISR ( < 0.001) groups related to healthy subjects. No significant differences were observed between the studied groups regarding thiol levels, antioxidant enzyme activities, and TAC. Multinomial logistic regression analysis showed that elevated serum levels of MDA (OR: 1.028, 95% CI: 1.008-1.048; = 0.006) and PAB (OR: 1.076, 95% CI: 1.017-1.139; = 0.011) were significantly associated with higher ISR risk; however, increased values of TAC (OR: 0.990, 95% CI: 0.982-0.999; = 0.030) were significantly associated with decreased ISR risk, while after adjustment for confounders, only SOD activity (OR: 0.0, 95% CI: 0.0-0.0; < 0.001) and PAB value (OR: 1.866, 95% CI: 1.856-1.900; < 0.001) showed association with ISR risk.

CONCLUSION

According to the present findings, some oxidative and antioxidative markers like PAB and SOD activity showed the potential in the prediction of ISR risk.

摘要

背景

支架内再狭窄(ISR)是支架植入后发生的重要临床并发症。尽管应用药物洗脱支架(DES),甚至使用抗血小板药物和他汀类药物等药物,都不能完全降低 ISR 的风险。由于此类患者数量持续增加,因此检测具有较高 ISR 风险的患者至关重要。此外,识别 ISR 的生化标志物可以为选择治疗这些患者的正确策略提供正确的视角。包括氧化应激(OS)在内的几种病理生理途径与 ISR 的进展有关。因此,本研究旨在评估氧化/抗氧化标志物与 ISR 之间的关系。

方法

这是一项病例对照研究,共纳入 21 例 ISR、26 例非 ISR(NISR)和 20 例健康对照者。采用比色法检测 OS 标志物,包括丙二醛(MDA)、巯基(GSH)、总抗氧化能力(TAC)和血清抗氧化酶如谷胱甘肽过氧化物酶(GPx)和超氧化物歧化酶(SOD)的活性。通过促氧化剂-抗氧化剂平衡(PAB)测定来评估整体氧化应激。

结果

与健康对照组相比,ISR 组 MDA 水平明显升高( = 0.004)。PAB 也表明,ISR(<0.001)和 NISR(<0.001)组与健康对照组相比,PAB 值明显升高。各组间巯基水平、抗氧化酶活性和 TAC 无显著差异。多变量逻辑回归分析显示,血清 MDA 水平升高(OR:1.028,95%CI:1.008-1.048; = 0.006)和 PAB 值升高(OR:1.076,95%CI:1.017-1.139; = 0.011)与较高的 ISR 风险显著相关;然而,TAC 值升高(OR:0.990,95%CI:0.982-0.999; = 0.030)与较低的 ISR 风险显著相关,而在调整混杂因素后,只有 SOD 活性(OR:0.0,95%CI:0.0-0.0;<0.001)和 PAB 值(OR:1.866,95%CI:1.856-1.900;<0.001)与 ISR 风险相关。

结论

根据本研究结果,一些氧化和抗氧化标志物,如 PAB 和 SOD 活性,在预测 ISR 风险方面具有潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/bde03c82229e/OMCL2022-3577761.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/c91139d821fd/OMCL2022-3577761.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/453d84d10008/OMCL2022-3577761.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/bde03c82229e/OMCL2022-3577761.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/c91139d821fd/OMCL2022-3577761.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/453d84d10008/OMCL2022-3577761.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7091/9256427/bde03c82229e/OMCL2022-3577761.003.jpg

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