Assessing the Protective Effects of Pioglitazone on Radiation-Induced Cardiac Injury in an In Vivo Model: A Biochemical and Histopathological Investigation.

IF 2.2 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Current Cardiology Reviews Pub Date : 2025-08-13 DOI:10.2174/011573403X388076250807224407

Fereshteh Talebpour Amiri, Fatemeh Jalali-Zefrei, Ehsan Zamani, Asma'a H Mohamed, Aynaz Sourati, Mohammad Shourmij, Mehrsa Majdayeen, Arsalan Salari, Zobin Souri, Soghra Farzipour

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引用次数: 0

Abstract

Introduction: RIHD is a significant complication in cancer radiotherapy, caused by oxidative stress and tissue damage. This study aimed to evaluate the protective effect of PGZ pretreatment against RIHD by assessing oxidative stress markers, enzyme levels, biochemical parameters, and cardiac tissue changes in a mouse model.

Materials & methods: 72 BALB/c mice were randomly divided into eight groups: control, PGZ (10, 20, and 30 mg/kg), IR (8 Gy), and IR + PGZ (at three doses). PGZ was administered daily for 10 days before exposure to RT on Day 11. 24 hours post-irradiation, cardiac tissues were analyzed for MDA levels, GPX and GSH concentrations, and serum markers including LDH and CPK. Histopathological examination was performed at 1 week and 1 month after irradiation to evaluate early inflammatory changes and late fibrosis.

Results: Results showed GPX activity increased by 28.2% and 48.4%, and GSH levels rose by 37.6% and 52.9% at doses of 20 and 30 mg/kg PGZ. MDA levels decreased by 40.35% and 52.63% at doses of 20 and 30 mg/kg, respectively. Serum LDH was reduced by 36.2% at 30 mg/kg. Tissue damage was significantly mitigated, with reductions of 88.9% at one week and 91.2% at one month. Fibrosis reduction was 23.5%, 41.5%, and 53.3% for 10, 20, and 30 mg doses.

Discussion: The findings highlight PGZ's potential to protect against RIHD via antioxidant enhancement; however, further clinical validation and exploration of long-term safety are essential.

Conclusions: PGZ shows promise in reducing RIHD by enhancing antioxidants and decreasing tissue damage, warranting further clinical investigation.

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评估吡格列酮对体内模型辐射性心脏损伤的保护作用：生化和组织病理学研究。

导读：RIHD是肿瘤放疗的重要并发症，由氧化应激和组织损伤引起。本研究旨在通过评估小鼠模型的氧化应激标志物、酶水平、生化参数和心脏组织变化来评估PGZ预处理对RIHD的保护作用。材料与方法：将72只BALB/c小鼠随机分为8组：对照组、PGZ组（10、20、30 mg/kg）、IR组（8 Gy）、IR + PGZ组（3个剂量）。PGZ每天服用10天，第11天暴露于RT。照射24小时后，检测心脏组织MDA水平、GPX和GSH浓度以及LDH和CPK等血清标志物。分别于照射后1周和1个月进行组织病理学检查，评估早期炎症变化和晚期纤维化。结果：20、30 mg/kg PGZ组GPX活性升高28.2%、48.4%，GSH水平升高37.6%、52.9%。20和30 mg/kg剂量组MDA水平分别下降40.35%和52.63%。30 mg/kg组血清LDH降低36.2%。组织损伤明显减轻，一周减少88.9%，一个月减少91.2%。10、20和30 mg剂量的纤维化减少率分别为23.5%、41.5%和53.3%。讨论：研究结果强调了PGZ通过抗氧化增强来预防RIHD的潜力；然而，进一步的临床验证和长期安全性的探索是必不可少的。结论：PGZ通过增强抗氧化剂和减少组织损伤来减少RIHD，值得进一步的临床研究。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Current Cardiology Reviews CARDIAC & CARDIOVASCULAR SYSTEMS-

CiteScore

3.70

自引率

10.50%

发文量

117

期刊介绍： Current Cardiology Reviews publishes frontier reviews of high quality on all the latest advances on the practical and clinical approach to the diagnosis and treatment of cardiovascular disease. All relevant areas are covered by the journal including arrhythmia, congestive heart failure, cardiomyopathy, congenital heart disease, drugs, methodology, pacing, and preventive cardiology. The journal is essential reading for all researchers and clinicians in cardiology.