Protective effects of limb remote ischemic per-conditioning on the heart injury induced by renal ischemic-reperfusion through the interaction of the apelin with the RAS/iNOS pathway.

IF 4.7 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-01-01 Epub Date: 2023-10-08 DOI:10.34172/bi.2023.27567

Sahar Janfeshan, Fatemeh Masjedi, Zeinab Karimi

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Abstract

Introduction: Remote ischemic conditioning upregulates endogenous protective pathways in response to ischemia-reperfusion injury. This study tested the hypothesis that limb remote ischemic per- conditioning (RIPerC) exerts cardioprotective effects via the renin-angiotensin system (RAS)/inducible nitric oxide synthase (iNOS)/apelin pathway.

Methods: Renal ischemia-reperfusion injury (I/R) was induced by bilateral occlusion of the renal pedicles for 60 minutes, followed by 24 hours of reperfusion; sham-operated rats served as controls. RIPerC was induced by four cycles (5 minutes) of limb ischemia-reperfusion along with bilateral renal ischemia. The functional disturbance was evaluated by renal (BUN and creatinine) and cardiac (troponin I and lactate dehydrogenase) injury biomarkers.

Results: Renal I/R injury increased renal and cardiac injury biomarkers that were reduced in the RIPerC group. Histopathological findings of the kidney and heart were also suggestive of amelioration injury-induced changes in the RIPerC group. Assessment of cardiac electrophysiology revealed that RIPerC ameliorated the decline in P wave duration without significantly affecting other cardiac electrophysiological changes. Further, renal I/R injury increased the plasma (322.40±34.01 IU/L), renal (8.27±1.10 mIU/mg of Protein), and cardiac (68.28±10.28 mIU/mg of protein) angiotensin-converting enzyme (ACE) activities in association with elevations in the plasma and urine nitrite (25.47±2.01 & 16.62±3.05 μmol/L) and nitrate (15.47±1.33 & 5.01±0.96 μmol/L) levels; these changes were reversed by RIPerC. Further, renal ischemia-reperfusion injury significantly (P=0.047) decreased the renal (but not cardiac) apelin mRNA expression, while renal and cardiac ACE2 (P<0.05) and iNOS (P=0.043) mRNA expressions were significantly increased compared to the sham group; these effects were largely reversed by RIPerC.

Conclusion: Our results indicated that RIPerC protects the heart against renal ischemia- reperfusion injury, likely via interaction of the apelin with the RAS/iNOS pathway.

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肢体远端缺血预处理通过apelin与RAS/iNOS通路的相互作用对肾缺血-再灌注心脏损伤的保护作用

远程缺血调节上调内源性保护通路以响应缺血再灌注损伤。本研究验证了肢体远端缺血预适应(RIPerC)通过肾素-血管紧张素系统(RAS)/诱导型一氧化氮合酶(iNOS)/apelin通路发挥心脏保护作用的假设。方法:双侧肾膜闭塞60分钟，再灌注24小时，诱导肾缺血再灌注损伤(I/R);假手术大鼠作为对照。在双侧肾缺血的同时进行4个周期(5分钟)的肢体缺血再灌注诱导RIPerC。通过肾脏(BUN和肌酐)和心脏(肌钙蛋白I和乳酸脱氢酶)损伤生物标志物评估功能障碍。结果:肾I/R损伤增加了肾和心脏损伤的生物标志物，而RIPerC组的生物标志物减少。肾脏和心脏的组织病理学结果也提示RIPerC组损伤引起的改变有所改善。心脏电生理评估显示，RIPerC改善了P波持续时间的下降，但对其他心脏电生理变化没有显著影响。肾I/R损伤使血浆(322.40±34.01 IU/L)、肾脏(8.27±1.10 mIU/mg Protein)和心脏(68.28±10.28 mIU/mg Protein)血管紧张素转换酶(ACE)活性升高，血浆和尿亚硝酸盐(25.47±2.01 & 16.62±3.05 μmol/L)和硝酸盐(15.47±1.33 & 5.01±0.96 μmol/L)水平升高;这些变化被RIPerC逆转了。与假手术组相比，肾缺血再灌注损伤显著(P=0.047)降低了肾脏(但不影响心脏)apelin mRNA的表达，肾脏和心脏ACE2 (P<0.05)和iNOS (P=0.043) mRNA的表达显著升高;这些影响在很大程度上被RIPerC逆转了。结论:我们的研究结果表明，RIPerC可能通过apelin与RAS/iNOS通路的相互作用，保护心脏免受肾缺血再灌注损伤。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464

期刊介绍： ACS Applied Bio Materials is an interdisciplinary journal publishing original research covering all aspects of biomaterials and biointerfaces including and beyond the traditional biosensing, biomedical and therapeutic applications. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrates knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important bio applications. The journal is specifically interested in work that addresses the relationship between structure and function and assesses the stability and degradation of materials under relevant environmental and biological conditions.