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Protective limb remote ischemic post-conditioning against high-intraocular-pressure-induced retinal injury in mice

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International Journal of Ophthalmology(English edition) 2022年第4期15卷 560-567页

作者： Qi-Jiang Zhu Lei Zhang Shuang-Yu Lyu Zhan-Jun Cui En-She Jiang Jun Wang School of Clinical Medicine Henan UniversityKaifeng 475001Henan ProvinceChina Henan International Joint Laboratory for Nuclear Protein Regulation Henan UniversityKaifeng 475001Henan ProvinceChina School of Basic Medical Sciences Henan UniversityKaifeng 475001Henan ProvinceChina Institute of Nursing and Health School of Nursing and HealthHenan UniversityKaifeng 475001Henan ProvinceChina

AIM: To determine whether limb remote ischemic postconditioning(LRIC) protects against high-intraocularpressure(IOP)-induced retinal injur y, and to identify underlying molecular mechanisms. METHODS: In mice, IOP was increased to 110 mm Hg for 50 min and LRIC applied to the unilateral leg for three occlusion cycles(5 min/release). Three animal groups(control, high IOP, and high IOP+LRIC) were arranged in this study. Plasma was collected from LRIC treated mice. Retinal histology, oxidative stress were determined by histological section staining and chemical kit. C/EBP homologous protein(CHOP), and Iba-1 parameters were evaluated by immunofluorescent staining and Western blot. RESULTS: The data showed that LRIC treatment alleviated the retinal histological disorganization and ganglion cell loss induced by high IOP. The CHOP, Iba-1 expression and oxidative stress marker also were inhibited by LRIC treatment. To further explore underlying mechanisms, plasma from LRIC treated animals was intravenously transfused into high-IOP animals. The results showed plasma injection decreased caspase 9 expression and DHE staining signals compared with that in high IOP retinas. CONCLUSION: These data suggest that LRIC treatments exert retinal protective effects against high-IOP *** humoral factors release into the circulation by LRIC may contribute to homeostatic protection by reducing monocyte infiltration and/or microglia activation.

关键词： retina ischemic conditioning high intraocular pressure

Impact of Acute Ischemia-Reperfusion Injury on Left Ventricular Pressure-Volume Relations in Dogs

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World Journal of Cardiovascular Diseases 2022年第4期12卷 236-249页

作者： John G. Kingma Denys Simard Jacques R. Rouleau Department of Medicine Faculty of Medicine Laval University Québec QC Canada

Objective: ischemic conditioning (IC) limits myocyte necrosis after acute myocardial ischemia-reperfusion;however, controversy persists regarding its potential to attenuate LV contractile dysfunction. Pressure-volume (P-V) loop analysis, via the load-insensitive conductance catheter method, was used to evaluate LV contractility, diastolic function, and ventriculo-arterial coupling. The goal of this study was to evaluate the ability of IC to improve post-ischemic recovery of LV contractile function. Methods: Twelve anesthetized dogs were randomly distributed to either the IC or the non-IC group;all dogs were subject to 60-min acute coronary occlusion followed by 180-min reperfusion. IC consisted of 4 repeated cycles of 5-min occlusion and 5-min reperfusion of the left main coronary artery. LV P-V relations were constructed under steady-state conditions (by inferior vena cava occlusion) at the beginning and end of the experiments;P-V loops were acquired at different time points before and during ischemia-reperfusion. Results: During ischemia and reperfusion, dP/dtmax decreased significantly compared to baseline in both groups;dP/dtmin, an indicator of the rate of LV relaxation rate was not affected for either group. Significant changes in several parameters of LV function including LVEF, SW, tPFR, ESV, and EDV caused by ischemia were also identified;none of these negative effects were resorbed, even in part, during reperfusion. Conclusions: Diminished LV contractile efficiency during systole and diastole produced by ischemia-reperfusion did not improve with IC pre-treatment despite significant endogenous protection against tissue necrosis.

关键词： ischemic conditioning Ischemia Reperfusion Ventricular Function Pressure-Volume Relations

Contribution of Myocyte Apoptosis to Myocardial Injury in an in Vivo Rabbit Preparation of Ischemia-Reperfusion

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World Journal of Cardiovascular Diseases 2022年第8期12卷 426-438页

作者： John G. Kingma Department of Medicine Faculty of Medicine Laval University Québec Canada

Objective: Exposure of the heart to repeated, brief episodes of coronary occlusion/reperfusion prevents lethal myocyte injury. Necrosis and apoptosis, two seemingly distinct mechanisms of cell death caused by ischemia could contribute independently to progressive loss of myocardium. Studies suggest that ischemic conditioning (IC) lessens myocyte injury by decreasing apoptosis. The goal of this study was to examine cell death in rabbit hearts subject to ischemia-reperfusion injury without (nIC) or with pretreatment by IC. Methods: In the control study, anesthetized, male rabbits (n = 4/group) underwent 30-min regional coronary occlusion (CO) and either 3, 6 or 24h reperfusion (REP). In the IC study, rabbits were pretreated by IC (2 cycles of 5-min CO and 10-min REP) before 30-min CO and subsequent REP. Additional groups were evaluated with 60, or 120-min CO followed by up to 96 h REP. Agarose electrophoresis was used to detect DNA laddering and poly (ADP-ribose) polymerase (PARP;chromatin bound nuclear DNA repair enzyme) was assessed in myocardial biopsies. Results: Genomic DNA from nIC and IC hearts showed no oligonucleosomal fragmentation. In addition, we did not detect any cleavage of PARP;however, myocardial PARP levels decreased when CO and REP durations were prolonged. Conclusion:Absence of genomic DNA fragmentation or PARP cleavage in an in vivo preparation of ischemia-reperfusion injury does not support the view that apoptosis contributes markedly to post-ischemic tissue necrosis.

关键词： Ischemia Reperfusion ischemic conditioning Necrosis Apoptosis DNA Fragmentation PARP Cleavage Rabbits

Induction of ischemic tolerance as a promising treatment against diabetic retinopathy

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Neural Regeneration Research 2014年第17期9卷 1581-1584页

作者： Ruth E.Rosenstein Diego C.Fernandez Laboratory of Retinal Neurochemistry and Experimental Ophthalmology Department of Human BiochemistrySchool of Medicine/CEFyBOUniversity of Buenos Aires/CONICET Present address:Johns Hopkins University Department of Biology

Diabetic retinopathy is a leading cause of acquired blindness, and it is the most common ischemic disorder of the retina. Available treatments are not very effective. Efforts to inhibit diabetic reti- nopathy have focused either on highly specific therapeutic approaches for pharmacologic targets or using genetic approaches to change expression of certain enzymes. However, it might be wise to choose innovative treatment modalities that act by multiple potential mechanisms. The resis- tance to ischemic injury, or ischemic tolerance, can be transiently induced by prior exposure to a non-injurious preconditioning stimulus. A complete functional and histologic protection against retinal ischemic damage can be achieved by previous preconditioning with non-damaging isch- emia. In this review, we will discuss evidence that supports that ischemic conditioning could help avert the dreaded consequences that results from retinal diabetic damage.

关键词： diabetic retinopathy ischemic tolerance retina ischemic injury ischemic conditioning