The Protective Effects of Melatonin, Vitamin E and Octreotide on Retinal Edema during Ischemia-Reperfusion in the Guinea Pig Retina

2002 ◽  
Vol 12 (6) ◽  
pp. 443-449 ◽  
Author(s):  
T. Yilmaz ◽  
S. Çelebi ◽  
A.Ş. Kükner
Keyword(s):  
Vitamin E ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Plexiform Layer ◽  
Retinal Ischemia ◽  
Control Group ◽  
Inner Plexiform Layer ◽  
Free Radical Damage ◽  
Microscopic Evaluation ◽  
Group 1

Purpose The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia-reperfusion (I/R) injury, and to determine whether melatonin, vitamin E and octreotide can protect retina from this injury. Methods The right eyes of 50 male guinea pigs weighing 500–600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (melatonin + I/R), group 4 (vitamin E + I/R) and group 5 (octreotide + I/R). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 10 mg/kg melatonin, 150 mg/kg vitamin E and 22 μg/kg octreotide respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 1.5 hours, then followed by reperfusion for 24 hours. Infections of all three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 μm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. Results The efficacy of each compound had the following relationships: melatonin>vitamin E>octreotide in preventing retinal damage by ischemia-reperfusion. The mean thickness of the inner plexiform layer was 13.3 ± 0.8 μm, 25.9 ± 2.0 μm, 20.0 ± 0.7 μm, 21.6 ± 0.7 μm, 23.9 ± 0.8 μm respectively in the control, I/R, I/R plus melatonin, I/R plus vitamin E and I/R plus octreotide groups. The thickness of the inner plexiform layer in group 1 (control) was significantly less than the other groups (p<0.001). The inner plexiform layer was thicker in the I/R group than with I/R plus melatonin, I/R plus vitamin E and I/R plus octreotide (all p <0.01). The inner plexiform layer was thicker in the I/R plus octreotide group than the I/R plus vitamin E and I/R plus melatonin groups both (p<0.05). Compared to the I/R plus melatonin group, the inner plexiform layer was significantly thicker in the I/R plus vitamin E group (p<0.05). Conclusions This study demonstrates a protective effect of melatonin, vitamin E and octreotide on the retina during retinal ischemia-reperfusion injury.

THE NEUROPROTECTIVE EFFECTS ON RETINAL STRUCTURE BY MINOCYCLINE IN A RAT MODEL OF HIGH IOP INDUCED RETINAL ISCHEMIA INJURY

2014 ◽  
Vol 40 (02) ◽  
pp. 83-87
Author(s):  
Pei-Yun Huang ◽  
Chung-Tien Lin
Keyword(s):  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Outer Nuclear Layer ◽  
Plexiform Layer ◽  
Retinal Ischemia ◽  
Control Group ◽  
Inner Plexiform Layer ◽  
Sprague Dawley ◽  
Neuroprotective Effects ◽  
Retinal Structure

The present study investigated the neuroprotective effect of minocycline, a microglial inhibitor, against the retinal ischemia–reperfusion (IR) injury in the rat. The retinal IR injury was induced in Sprague–Dawley (SD) rats by infusing normal saline into anterior chamber of eye to create a higher intraocular pressure (IOP) than blood pressure for 45 min. Minocycline (45 and 90 mg/kg/day) was administered intraperitoneally to rats receiving IR injury. The neuroprotective effects were evaluated by morphometrical histology analysis 7 days after ischemia. The data was compared with the groups treated with saline and methylprenisolone (MP, 30 mg/kg, IV). The results showed that the retinal inner plexiform layer/outer nuclear layer (IPL/ONL) ratio was reduced following IR damage compared with that in the normal control. The IPL/ONL ratio was reduced to 43.5% in the IR-control group, 93.3% and 93.6% in the Mino-45 and Mino-90 group. The IPL/ONL ratio was preserved to 95.7% in the MP group. These results suggest that minocycline and methylprednisolone showed significantly good neuroprotective effects demonstrated in retinal histology of the rats under retinal IR injury.

scholarly journals Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury

2017 ◽  
Vol 74 (1) ◽  
pp. 105
Author(s):  
Razvan Andrei CODEA ◽  
Mircea MIRCEAN ◽  
Sidonia Alina BOGDAN ◽  
Andras Laszlo NAGY ◽  
Alexandra BIRIS ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Experimental Model ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Control Group ◽  
Tubular Injury ◽  
Group 2 ◽  
Group 1

The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects

scholarly journals Transneuronal Degeneration in the Visual Pathway of Rats following Acute Retinal Ischemia/Reperfusion

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yanyan Fu ◽  
Tu Hu ◽  
Qianyue Zhang ◽  
Shuhan Meng ◽  
Ying Lu ◽  
...  
Keyword(s):  
Visual Function ◽  
Ischemia Reperfusion ◽  
Plexiform Layer ◽  
Signal Propagation ◽  
Retinal Ischemia ◽  
Visual Pathways ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Inner Plexiform Layer ◽  
Transneuronal Degeneration ◽  
Neuronal Soma

The maintenance of visual function not only requires the normal structure and function of neurons but also depends on the effective signal propagation of synapses in visual pathways. Synapses emerge alterations of plasticity in the early stages of neuronal damage and affect signal transmission, which leads to transneuronal degeneration. In the present study, rat model of acute retinal ischemia/reperfusion (RI/R) was established to observe the morphological changes of neuronal soma and synapses in the inner plexiform layer (IPL), outer plexiform layer (OPL), and dorsal lateral geniculate nucleus (dLGN) after retinal injury. We found transneuronal degeneration in the visual pathways following RI/R concretely presented as edema and mitochondrial hyperplasia of neuronal soma in retina, demyelination, and heterotypic protein clusters of axons in LGN. Meanwhile, small immature synapses formed, and there are asynchronous changes between pre- and postsynaptic components in synapses. This evidence demonstrated that transneuronal degeneration exists in RI/R injury, which may be one of the key reasons for the progressive deterioration of visual function after the injury is removed.

scholarly journals Interleukin-35 Suppresses Pyroptosis and Protects Neuronal Death in Retinal Ischemia/Reperfusion Injury

2021 ◽  
Author(s):  
Bingying Lin ◽  
Yangyang Li ◽  
Nan Jiang ◽  
Siyu Huang ◽  
Wenru Su ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Plexiform Layer ◽  
Glucose Deprivation ◽  
Inner Plexiform Layer

Abstract Background: Retina ischemia-reperfusion (I/R) is a pathological process in many eye disorders. Neuroinflammation and cell pyroptosis have been recognized as important in the pathogenesis of tissue damage in retina I/R. Interleukin (IL)-35 is a novel heterodimeric cytokine that exhibits anti-inflammatory activity in virous autoimmune diseases, but its role in retina I/R and the underlying molecular mechanisms remain unexplored. This study investigated the effect of IL-35 on retina I/R and the inhibition of pyroptosis and neuronal death.Methods: A murine retina I/R model was used to explore the neuroprotective effect of IL-35 recombinant protein in vivo. The primary murine microglial cells of pyroptosis and the retinal ganglion cells (RGCs) of oxygen and glucose deprivation/reoxygenation (OGD/R) models were employed to test the anti-pyroptotic and anti-apoptotic effects of IL-35 in vitro.Result: We found that IL-35 decreases retinal damage, RGC death, and inner plexiform layer (IPL) thinning in mice with retinal I/R injury, with significant attenuation of pyroptosis in the retina. The data also demonstrated the anti-pyroptosis action of IL-35 in primary microglia stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Furthermore, primary RGC apoptosis induced by OGD/R was directly suppressed by IL-35, and the IL-35-mediated neuroprotection was abrogated when miR-21 was blocked.Conclusion: Our findings identify potential underlying mechanisms of RGC apoptosis and suggest a new therapeutic target, IL-35, which exerts a robust neuroprotective effect against retina I/R.

Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Neurological Deficit ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

scholarly journals Melatonin attenuates ovarian ischemia reperfusion injury in rats by decreasing oxidative stress index and peroxynitrite

2020 ◽  
Vol 50 (6) ◽  
pp. 1513-1522
Author(s):  
Şenol KALYONCU ◽  
Bülent YILMAZ ◽  
Mustafa DEMİR ◽  
Meltem TUNCER ◽  
Zehra BOZDAĞ ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Index ◽  
Oxidative Stress Index ◽  
Group 6 ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Background/aim: To evaluate the protective effect of melatonin on ovarian ischemia reperfusion injury in a rat model. Materials and methods: Forty-eight rats were separated equally into 6 groups. Group 1: sham; Group 2: surgical control with 3-h bilateral ovarian torsion and detorsion; Group 3: intraperitoneal 5% ethanol (1 mL) just after detorsion (as melatonin was dissolved in ethanol); Group 4: 10 mg/kg intraperitoneal melatonin 30 min before 3-h torsion; Group 5:10 mg/kg intraperitoneal melatonin just after detorsion; Group 6:10 mg/kg intraperitoneal melatonin 30 min before torsion and just after detorsion. Both ovaries and blood samples were obtained 7 days after detorsion for histopathological and biochemical analysis.Results: In Group 1, serum levels of total oxidant status (TOS) (μmol H2O2 equivalent/g wet tissue)were significantly lower than in Group2 (P = 0.0023), while tissue TOS levels were lower than in Group 3 (P = 0.0030). Similarly, serum and tissue levels of peroxynitrite in Group 6were significantly lower than those ofGroup 2 (P = 0.0023 and P = 0.040, respectively). Moreover, serum oxidative stress index (OSI) (arbitrary unit) levels were significantly increased in Group 2 when compared to groups 1 and 6 (P = 0.0023 and P= 0.0016, respectively) and in Group 3 with respect to groups 1, 4, 5, and 6 (P = 0.0023, P = 0.0026, P = 0.0008, and P = 0.0011, respectively). Furthermore, there was a significant decrease in histopathological scores including follicular degeneration, vascular congestion, hemorrhage, and inflammation in the melatonin and sham groups in comparison with control groups. Additionally, primordial follicle count was significantly higher in Group 6 than in Group 2 (P = 0.0002).Conclusion: Melatonin attenuates ischemia reperfusion damage in a rat torsion/detorsion model by improving histopathological and biochemical findings including OSI and peroxynitrite.

Abstract 138: Remote Ischemic Postconditioning Alleviates Postresuscitation Inflammatory Response and Pulmonary Edema in a Porcine Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jiefeng Xu ◽  
Sen Ye ◽  
Zilong Li ◽  
Moli Wang ◽  
Zhengquan Wang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Inflammatory Response ◽  
Pulmonary Edema ◽  
Porcine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Multiple Organ ◽  
Control Group ◽  
Lung Water

Introduction: Systemic ischemia-reperfusion injury produced by CA and resuscitation can result in severe post-cardiac arrest syndrome; which includes systemic inflammatory response and multiple organ dysfunction syndrome such as acute pulmonary edema. We previously demonstrated that remote ischemic post-conditioning (RIpostC) improved post-resuscitation myocardial and cerebral function in a rat model of CA. In this study, we investigated the effects of RIpostC on inflammatory response and pulmonary edema after CPR in a porcine model. Hypothesis: RIpostC would alleviate post-resuscitation inflammatory response and pulmonary edema in a porcine model of CA. Methods: Fourteen male domestic pigs weighing 37 ± 2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 10 mins. The animals were then randomized to receive RIpostC or control. Coincident with the start of CPR, RIpostC was induced by four cycles of 5 mins of limb ischemia and then 5 mins of reperfusion. Defibrillation was attempted after 5 mins of CPR. The resuscitated animals were monitored for 4 hrs and observed for an additional 68 hrs. Results: Six of the seven animals in each group were successfully resuscitated. After resuscitation, significantly lower levels of tumor necrosis factor-α and interleukin-6 were measured in the animals that received RIpostC when compared with the control group. Post-resuscitation extra-vascular lung water index was lower in the RIpostC group than in the control group; in which the differences were significant at 2,3 and 4 hrs (Table). Conclusion: In a porcine model of CA, RIpostC significantly alleviates post-resuscitation inflammatory response and pulmonary edema.

scholarly journals Preconditioning with L-alanyl-L-glutamine in a Mongolian Gerbil model of acute cerebral ischemia/reperfusion injury

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 14-20 ◽  
Author(s):  
Vilma Leite de Sousa Pires ◽  
José Reniclebson Feitosa de Souza ◽  
Sergio Botelho Guimarães ◽  
Antonio Ribeiro da Silva Filho ◽  
José Huygens Parente Garcia ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Femoral Vein ◽  
Control Group ◽  
Mongolian Gerbils ◽  
Cerebral Tissue ◽  
Arterial Blood ◽  
Cerebral Ischemia Reperfusion ◽  
Acute Cerebral Ischemia

PURPOSE: To investigate the effect of L-alanyl-L-glutamine (L-Ala-Gln) preconditioning in an acute cerebral ischemia/reperfusion (I/R) model in gerbils. METHODS: Thirty-six Mongolian gerbils (Meriones unguiculatus), (60-100g), were randomized in 2 groups (n=18) and preconditioned with saline 2.0 ml (Group-S) or 0.75g/Kg of L-Ala-Gln, (Group-G) administered into the femoral vein 30 minutes prior to I/R. Each group was divided into three subgroups (n=6). Anesthetized animals (urethane, 1.5g/Kg, i.p.) were submitted to bilateral occlusion of common carotid arteries during 15 minutes. Samples (brain tissue and arterial blood) were collected at the end of ischemia (T0) and after 30 (T30) and 60 minutes (T60) for glucose, lactate, myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), glutathione (GSH) assays and histopathological evaluation. RESULTS: Glucose and lactate levels were not different in studied groups. However glycemia increased significantly in saline groups at the end of the reperfusion period. TBARS levels were significantly different, comparing treated (Group-G) and control group after 30 minutes of reperfusion (p<0.05) in cerebral tissue. Pretreatment with L-Ala-Gln promoted a significant increase in cerebral GSH contents in Group-G at T30 (p<0.001) time-point compared with Group-S. At T30 and T60, increased levels of GSH occurred in both time-points. There were no group differences regarding MPO levels. Pyknosis, presence of red neurons and intracellular edema were significantly smaller in Group-G. CONCLUSION: Preconditioning with L-Ala-Gln in gerbils submitted to cerebral ischemia/reperfusion reduces oxidative stress and degeneration of the nucleus (pyknosis) and cell death (red neurons) in the cerebral tissue.

scholarly journals The protective effect of L-arginine, tadalafil, and their combination in rat testes after ischemia and reperfusion injury

2017 ◽  
Vol 11 (1-2) ◽  
pp. 19 ◽  
Author(s):  
Gokhun Ozmerdiven ◽  
Burhan Coskun ◽  
Onur Kaygisiz ◽  
Berna Aytac Vuruskan ◽  
Burak Asiltas ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Combination Group ◽  
Control Group ◽  
Ischemia And Reperfusion ◽  
Contralateral Testis ◽  
Treatment Groups ◽  
Testis Torsion

Introduction: Nitric oxide (NO) plays an important role in the ischemia and reperfusion process. In this study, we aimed to examine the effect of L-arginine, tadalafil, and their combination for preventionof the ischemia reperfusion injury after testis torsion in rats.Methods: A total of 40 adult, male Sprague-Dawley rats were allocated into five groups. Three hours of left testicular torsion was performed in each group, excluding the control group. While the ischemia reperfusion (I/R) group had no treatment, I/R + Arg group received L-arginine, I/R + Td group received tadalafil and I/R + Arg + Td group received tadalafil and L-arginine 30 minutes before the detorsion. Then the left testis was untwisted for four hours of reperfusion. After bilateral orchiectomy, lipid peroxidation (LPx) and glutathione (GSH) activities were examined in testicular tissue.Spermatogenesis was evaluated with Johnsen’s score.Results: LPx levels of the I/R group were found to be significantly higher than for groups that received drugs for both testes (p<0.001). GSH levels of the combination group were higher than I/R group inipsilateral testis (p<0.01) and it was significantly higher than other groups for contralateral testis (p<0.001 for I/R group, p<0.01 for I/R + Arg, p<0.05 for I/R + Td). Mean Johnsen’s score of the I/Rgroup was found to be significantly lower than treatment groups in ipsilateral testis (p<0.001 for I/R + Arg + Td group, p<0.01 for other treatment goups) and contralateral testis (p<0.001). The meanJohnsen score of the combination group was significantly higher than that of other treatment groups in ipsilateral testis (p<0.05) and it was significantly higher than in the I/R + Td group in the contralateral testis (p<0.05).Conclusions: L-arginine, tadalafil, and combination of these two molecules showed protective effect against ischemia/reperfusion injury for both testes after unilateral testis torsion.

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