The Protective Effect of Carvacrol Against Isoproterenol-Induced Cardiotoxicity in Rats.

IF 1.5 Q2 MEDICINE, GENERAL & INTERNAL
Seyhan Ayık, Hamza Dogukan Erfirat, Onural Ozhan, Mehmet Gunata, Azibe Yildiz, Merve Durhan, Yilmaz Cigremis, Hakan Parlakpinar
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引用次数: 0

Abstract

Objective: Isoproterenol (ISO)-induced myocardial injury involves oxidative stress (OS) and inflammation. Given carvacrol (CAR)'s antioxidant and cardioprotective properties, we aimed to investigate its protection against ISO-induced myocardial injury in rats.

Methods: Thirty male Wistar albino rats were assigned to three groups: Control; ISO (100 mg/kg, subcutaneous, for 2 days); and CAR+ISO (CAR 50 mg/kg/day, orally at 9:00, for 7 days + ISO at 16:00 on days 6-7). CAR and ISO doses were chosen based on prior evidence of CAR's antioxidant effects and ISO-induced oxidative cardiac stress. Diastolic and mean arterial pressures, corrected QT interval (QTc), T-wave changes, and serum troponin I levels were assessed. Cardiac OS biomarkers [malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)] and histopathology were evaluated.

Results: ISO markedly increased troponin I from 43.9 to 508.9 ng/mL and slightly reduced GSH from 1502.4 to 1330 nmol/g wet tissue and SOD from 1080.25 to 1010.34 U/g protein. ISO markedly reduced MDA (95.30 to 71.78 nmol/g wet tissue at 535 nm; 77.49 to 61.24 nmol/g wet tissue at 520 nm), likely due to depletion of lipid peroxidation substrates caused by excessive reactive oxygen species production, while slightly increasing CAT (132.66 to 162.04 K/g protein), possibly as a compensatory response. QTc and histopathological scores increased significantly; histopathological components were cardiomyocyte degeneration (CD) (range, 0.0 to 2.0), interstitial edema (IE) (range, 0.0 to 2.0), and granulation tissue (GT) (range, 0.0 to 1.0). CAR attenuated electrocardiographic abnormalities, significantly reduced troponin I (from 508.9 to 38.05 ng/mL), and restored GSH (from 1330 to 1396.8), SOD (from 1010.34 to 1094.42), and CAT (from 162.04 to 135.58). CAR significantly ameliorated histopathological scores: CD (2.0 to 1.0), IE (2.0 to 1.0), and GT (1.0 to 0.0).

Conclusions: CAR exerts protective effects against ISO-induced myocardial injury via antioxidant, membrane-stabilizing, and possible anti-arrhythmic properties. These findings support the therapeutic potential of CAR in OS-mediated cardiac pathologies and warrant further investigation in chronic and molecularly targeted models.

香芹酚对异丙肾上腺素所致大鼠心脏毒性的保护作用。
目的:异丙肾上腺素(ISO)引起的心肌损伤涉及氧化应激(OS)和炎症反应。鉴于carvacrol (CAR)的抗氧化和心脏保护作用,我们旨在研究其对iso诱导的大鼠心肌损伤的保护作用。方法:雄性Wistar白化大鼠30只,随机分为3组:对照组;ISO (100mg /kg,皮下,持续2天);CAR+ISO (CAR 50 mg/kg/天,9:00口服,连续7天+ISO在第6-7天的16:00)。CAR和ISO剂量的选择是基于CAR的抗氧化作用和ISO诱导的氧化性心脏应激的先前证据。评估舒张压和平均动脉压、校正QT间期(QTc)、t波变化和血清肌钙蛋白I水平。评估心脏OS生物标志物[丙二醛(MDA)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)]和组织病理学。结果:ISO使肌钙蛋白I从43.9增加到508.9 ng/mL, GSH从1502.4减少到1330 nmol/g, SOD从1080.25减少到1010.34 U/g。ISO显著降低了MDA (535 nm时为95.30至71.78 nmol/g湿组织;520 nm时为77.49至61.24 nmol/g湿组织),可能是由于过量活性氧产生导致脂质过氧化底物耗损,而CAT(132.66至162.04 K/g蛋白质)略有增加,可能是一种代偿反应。QTc和组织病理学评分显著升高;组织病理学成分为心肌细胞变性(CD)(范围:0.0 ~ 2.0)、间质水肿(IE)(范围:0.0 ~ 2.0)和肉芽组织(GT)(范围:0.0 ~ 1.0)。CAR可减轻心电图异常,显著降低肌钙蛋白I(从508.9降至38.05 ng/mL),恢复GSH(从1330降至1396.8)、SOD(从1010.34降至1094.42)和CAT(从162.04降至135.58)。CAR显著改善了组织病理学评分:CD(2.0至1.0),IE(2.0至1.0)和GT(1.0至0.0)。结论:CAR通过抗氧化、膜稳定和可能的抗心律失常特性对iso诱导的心肌损伤具有保护作用。这些发现支持了CAR在os介导的心脏病变中的治疗潜力,值得在慢性和分子靶向模型中进一步研究。
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
Medeniyet medical journal
Medeniyet medical journal Medicine-Medicine (all)
CiteScore
1.70
自引率
0.00%
发文量
88
审稿时长
5 weeks
期刊介绍: The Medeniyet Medical Journal (Medeniyet Med J) is an open access, peer-reviewed, and scientific journal of Istanbul Medeniyet University Faculty of Medicine on various academic disciplines in medicine, which is published in English four times a year, in March, June, September, and December by a group of academics. Medeniyet Medical Journal is the continuation of Göztepe Medical Journal (ISSN: 1300-526X) which was started publishing in 1985. It changed the name as Medeniyet Medical Journal in 2015. Submission and publication are free of charge. No fees are asked from the authors for evaluation or publication process. All published articles are available online in the journal website (www.medeniyetmedicaljournal.org) without any fee. The journal publishes intradisciplinary or interdisciplinary clinical, experimental, and basic researches as well as original case reports, reviews, invited reviews, or letters to the editor, Being published since 1985, the Medeniyet Med J recognizes that the best science should lead to better lives based on the fact that the medicine should serve to the needs of society, and knowledge should transform society. The journal aims to address current issues at both national and international levels, start debates, and exert an influence on decision-makers all over the world by integrating science in everyday life. Medeniyet Med J is committed to serve the public and influence people’s lives in a positive way by making science widely accessible. Believing that the only goal is improving lives, and research has an impact on people’s lives, we select the best research papers in line with this goal.
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