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

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Janfeshan Sahar; Masjedi Fatemeh; Karimi Zeinab

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Journal: BIOIMPACTS Year:2024 | Volume:14 | Issue:2 Page(s): 1-12

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Title

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

Author(s)

Janfeshan Sahar | Masjedi Fatemeh | Karimi Zeinab | Issue Writer Certificate

Keywords

Limb remote ischemic per-conditioning

Renal ischemia reperfusion

Myocardial injury

Apelin

Renin-angiotensin system

iNOS

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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