oxytocin and Reperfusion-Injury

This study aimed to demonstrate the effects of oxytocin on penile tissues in ischemia-reperfusion injury developed after priapism.. Forty Wistar Albino strain male rats were divided into four groups. The control group (n = 10) was not intervened. In Group 2, a rat model of priapism was constructed and maintained for 1 h. In Group 3, reperfusion was ensured for 30 min following priapism. Rats in Group 4 rats were given oxytocin 30 min before the induction of reperfusion following priapism. All rats were penectomized, and adequate amounts of blood sample were drawn. Inflammation, vasocongestion, desquamation, and edema in penile tissue were scored between 0 and 3 points (0: normal, 1: mild, 2: moderate, 3: severe) to evaluate the severity of tissue damage. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the levels of malondialdehyde (MDA), and nitric oxide (NO) in blood samples were determined spectrophotometrically.. In histopathological examination, statistically significant positive changes were detected in vasocongestion, inflammation, desquamation, and edema scores in Group 4 than in Group 2 and Group 3 (p < 0.001). Biochemical test results revealed that NO levels were significantly lower in Group 4 than in Group 3 (p < 0.001). Serum GSH-Px activities in Group 4 significantly increased when compared with the other groups 2 and 3 (p = 0.002, p = 0.001, respectively). There was no statistical difference among the groups regarding SOD activities and MDA levels (p > 0.05).. Oxytocin protected against priapism-induced ischemia-reperfusion injury developed in cavernosal tissue as observed based on histopathological and biochemical evidence. Although this is an experimental study, oxytocin can be thought as an alternative drug in the treatment of priapism.

Topics: Animals; Disease Models, Animal; Glutathione Peroxidase; Male; Malondialdehyde; Nitric Oxide; Oxytocin; Penis; Priapism; Protective Factors; Rats; Rats, Wistar; Reperfusion Injury; Severity of Illness Index; Superoxide Dismutase; Time Factors

Different mechanisms will be activated during ischemic stroke. Calpain proteases play a pivotal role in neuronal death after ischemia damage through apoptosis. Anti-apoptotic activities of the oxytocin (OT) in different ischemic tissues were reported in previous studies. Recently, a limited number of studies have noted the protective effects of OT in the brain. In the present study, the neuroprotective potential of OT in an animal model of transient middle cerebral artery occlusion (tMCAO) and the possible role of calpain-1 in the penumbra region were assessed.. Adult male Wistar rats underwent 1 hour of tMCAO and were treated with nasal administration of OT. After 24 hours of reperfusion, infarct size was evaluated by triphenyltetrazolium chloride. Immunohistochemical staining and Western blotting were used to examine the expression of calpain-1. Nissl staining was performed for brain tissue morphology evaluation.. OT reduced the infarct volume of the cerebral cortex and striatum compared with the ischemia control group significantly (P < .05). Calpain-1 overexpression, which was caused by ischemia, decreased after OT administration (P < .05). The number of pyknotic nuclei in neurons increased dramatically in the ischemic area and OT attenuated the apoptosis of neurons in the penumbra region (P < .01).. We provided evidence for the neuroprotective role of OT after tMCAO through calpain-1 attenuation.

Topics: Administration, Intranasal; Animals; Apoptosis; Brain; Calpain; Disease Models, Animal; Infarction, Middle Cerebral Artery; Male; Neurons; Neuroprotective Agents; Nitric Oxide; Oxytocin; Rats, Wistar; Receptors, Oxytocin; Reperfusion Injury; Signal Transduction; Time Factors

We aimed to demonstrate the effectiveness of oxytocin on the testes for treating ischemia-reperfusion injury.. A total of 24 male Wistar albino rats weighing 250-320 g were used. The rats were randomized into three groups of eight rats. Group 1 was assessed as the control group. In Group 2 rats, testicular torsion was first performed, followed by testicular detorsion to induce reperfusion injury. In Group 3, following testicular torsion and detorsion, oxytocin was administered before inducing reperfusion. Testicular tissues were histologically evaluated, spermatogenic parameters were assessed using the Johnsen scoring system, and the mean Johnsen score was calculated.. Histological tests revealed significantly different results between the testicular torsion group and the oxytocin-treated torsion and control groups as well as between the oxytocin-treated torsion group and the control and testicular torsion groups (p=0.010 and 0.012, respectively). Biochemical test results revealed that superoxide dismutase and glutathione peroxidase levels were significantly lower in Group 2 than in Group 1 (p=0.007 and 0.007, respectively). Malondialdehyde and nitric oxide levels were significantly lower in Group 3 than in Group 2 (p=0.017 and 0.014, respectively).. These results indicate that oxytocin can be considered as an alternative agent for treating testicular torsion in clinical practice to minimize tissue damage.

Topics: Animals; Male; Oxytocin; Random Allocation; Rats; Rats, Wistar; Reperfusion Injury; Spermatic Cord Torsion

Oxytocin (OT) has an anti-inflammatory and antioxidant effect in the different inflammatory models. The current study aimed to evaluate the protective function of OT in renal and hepatic damages triggered by renal ischemia/reperfusion (IR) in rats. Moreover, the effect of NG-nitro-l-arginine methyl ester (l-NAME) was investigated on the kidney and liver functions in renal IR model.. Twenty-four rats were divided into four groups (six rats each) as follows: (1) Sham-operated group; (2) Renal IR group; (3) Renal IR+OT group; (4) Renal IR+OT+l-NAME. OT (1 mg/kg, i.p.) was administered 30 min prior to the induced ischemia and was repeated immediately before the reperfusion period. l-NAME (10 mg/kg, i.p.) was given 45 min before IR injury.. The results revealed that OT significantly attenuated the IR-induced elevations in the serum urea, creatinine, liver transaminases, and TNF-α levels, while nitric oxide (NO) and Bcl-2 levels were significantly increased compared with the IR group. OT also significantly compensated the decrease in the total antioxidant capacities (TAC) and lowered the elevated malondialdehyde (MDA) levels that were observed with renal IR in the renal and hepatic tissues.. In conclusion, OT ameliorates renal and hepatic damages triggered by renal IR, and this defense involves the suppression of inflammation and apoptosis with regulation of oxidant-antioxidant status. In addition, administration of l-NAME prior to OT partially reversed the protective effect of OT ensuring that one of the protective effects of OT was through the NO production.

Topics: Animals; Creatinine; Kidney; Liver; Male; Malondialdehyde; NG-Nitroarginine Methyl Ester; Nitric Oxide; Oxytocin; Rats; Reperfusion Injury; Tumor Necrosis Factor-alpha; Urea

Ischemia/reperfusion (I/R) injuries result in damage to endothelial and parenchymal cells. Oxytocin (OXY) stimulates uterine contraction during parturition and myoepithelial cells during suckling. OXY has been used as a protective antioxidant. Kisspeptin plays a key role in the central control of reproductive functions and onset of puberty. Recent studies show that these reproductive hormones have protective potential as antioxidant. The aim of this study is to investigate the potential protective effects of Kisspeptin and OXY as antioxidants on I/R injured ovary and uterus of female rats.. Rats were separated into five groups. Group 1, is control group; Group 2, rats were subjected to ischemia followed by reperfusion. Group 3, OXY administration 30 min prior to I/R applied rats; Group 4, Kisspeptin administration 30 min prior to I/R applied rats; Group 5, OXY and Kisspeptin administration 30 min prior to I/R. Ovary and uterus were removed for histopathological and biochemical observations. Malondialdehyde, glutathione levels, and superoxide dismutase activities were analyzed in order to observe antioxidant potential of OXY and Kisspeptin. Hematoxylin and Eosin staining was applied for histopathologic scoring.. Stromal and granulosa cells in ovary, endometrial cells in uterus were damaged in I/R group. The cellular damage of ovary and uterus were reduced in OXY and Kisspeptin administered I/R group when compared to only Kisspeptin injected I/R group and I/R group. There is no significant difference between OXY and OXY + Kisspeptin injected I/R groups. MDA levels were decreased in Kisspeptin and/or Oxytocin applied I/R group compared to I/R group. SOD activity and GSH levels were increased in Kisspeptin and/or OXY applied I/R group compared to I/R group.. The present results suggest that exogenous application of oxytocin and kisspeptin can have antioxidant effects on the uterus and ovary.

Topics: Animals; Antioxidants; Female; Glutathione; Kisspeptins; Malondialdehyde; Ovary; Oxidative Stress; Oxytocin; Rats; Rats, Wistar; Reperfusion Injury; Superoxide Dismutase; Uterus

Oxytocin (OT), a neurohypophysial nonapeptide, plays dual role as a neurotransmitter/neuromodulator and a hormone. It has also well known protective properties against ischemia/reperfusion organ damage. This study investigated the effect of OT on experimentally induced ovarian torsion/de-torsion ischemia/reperfusion (I/R) injury in rats. Sprague-Dawley rats were assigned to five treatment groups (n=7/group): Group 1, sham-operated; Group 2, torsion; Group 3, 80 IU/kg of OT administration 30 min prior to torsion; Group 4, torsion/de-torsion; and Group 5, torsion followed by 80 IU/kg of OT administration 30 min prior to de-torsion. OT administration significantly decreased the tissue malondialdehyde (MDA) levels in both the torsion and OT group (Group 3), and torsion/de-torsion OT group (Group 5) in comparison with the torsion-only group (Group 2) and torsion/de-torsion group (Group 4). Histopathological finding scores including follicular degeneration, edema, hemorrhage, vascular congestion, and infiltration by inflammatory cells were found to be significantly decreased in the torsion and OT group (Group 3), and torsion/de-torsion OT group (Group 5) when compared with the torsion-only group (Group 2) and torsion/de-torsion group (Group 4). In conclusion, these results, verified with histopathologic evaluation and biochemical assays, suggest a probable protective role for OT in ischemia and I/R injury in rat ovaries.

Topics: Animals; Female; Lipid Peroxidation; Malondialdehyde; Ovary; Oxidative Stress; Oxytocin; Rats, Sprague-Dawley; Reperfusion Injury

Oxytocin (OXY) is a well-known nonapeptide that functions in reproduction. It is also known as an antioxidant in several organs. However, little is about its role in the protection of tissue against ischemia/reperfusion injury in skeletal muscle. The aim of this study was to evaluate the protective and therapeutic antioxidant effect of oxytocin in skeletal muscle during ischemia/reperfusion (I/R) injury.. Rats were divided into 4 groups. Hindlimb ischemia was achieved by clamping the common femoral artery in 3 of the groups, but not a control group. OXY was injected before ischemia in the preoperative (preop) I/R + OXY group and after the onset of ischemia in the postoperative (postop) I/R + OXY group. Saline solution was injected in the I/R group. Limbs were rendered ischemic for 90 min. At the end of 90-min reperfusion period, skeletal muscle tissue samples were taken from the ischemic muscle for evaluation at light and transmission electron microscopic levels. Biochemical analysis was done for malonedialdehyde and glutathione levels. Caspase immunohistochemistry was applied for apoptosis.. The light- and electron-microscopic scores of the OXY-treated groups were significantly lower than in the I/R group. The degree of tissue damage was ameliorated in the OXY-treated groups. The number of apoptotic cells was decreased in the OXY-treated groups compared with the I/R group. In OXY-treated groups, the malonedialdehyde level was lower than in the I/R group. Glutathione levels were found to be increased in the OXY-treated groups compared with the I/R group.. Oxytocin has a protective effect against I/R injury in skeletal muscle and may reduce the incidence of compartment syndrome.

Topics: Animals; Antioxidants; Caspase 3; Glutathione; Hindlimb; Lipid Peroxidation; Malondialdehyde; Microscopy, Electron, Transmission; Muscle, Skeletal; Oxytocin; Rats; Rats, Wistar; Reperfusion Injury

Oxytocin (OXY), a well-known nonapeptide, plays a crucial role in reproduction, and has effects on modulating the immune and inflammatory processes in living organisms as well. Recently it is also known as an antioxidant in several organs. The present study aims to demonstrate the protective effect of OXY against ischemia/reperfusion (I/R) injury in urinary bladder tissue. Abdominal aorta of rats, were clamped to perform urinary bladder ischemia. OXY (0.5 μg/kg) was injected intraperitoneally before ischemia in I/R+OXY group, whereas the vehicle solution was injected to I/R group. At the end of reperfusion, tissue samples from urinary bladder were processed for histochemical, ultrastructural and biochemical analysis. Tissue sections were stained by toluidine blue for mast cell counting and hematoxylin-eosin for histopathology. In addition, malondialdehyde (MDA) and glutathione (GSH) levels were determined biochemically. The results demonstrated that there was an extreme damage at urothelium, dilatation of intercellular junctions, inflammatory cell infiltration in I/R group. I/R+OXY group demonstrated a reduction in the severity of urinary bladder damage. According to mast cell counting results, both granulated and degranulated mast cells were decreased in I/R+OXY group compared to I/R group. The mean MDA level was higher in I/R group compared to control and lower in I/R+OXY group compared to I/R group. GSH level reduced in I/R group compared to the control and increased in I/R+OXY group compared to I/R group. In conclusion, oxytocin, as confirmed by histological evaluation and biochemical assays has a potential protective effect in the urinary bladder tissue against ischemia/reperfusion injury.

Topics: Animals; Aorta, Abdominal; Glutathione; Malondialdehyde; Oxytocin; Rats; Reperfusion Injury; Urinary Bladder; Urothelium

The aim of the present study was to reveal the effect of liver ischemia–reperfusion injury (LIRI) on the activity of selected neuronal phenotypes in rat brain by applying dual Fos-oxytocin (OXY), vasopressin (AVP), tyrosine hydroxylase (TH), phenylethanolamine N-methyltransferase (PNMT), corticoliberine (CRH), and neuropeptide Y (NPY) immunohistochemistry. Two liver ischemia–reperfusion models were investigated: (i) single ligation of the hepatic artery (LIRIa) for 30 min and (ii) combined ligation of the portal triad (the common hepatic artery, portal vein, and common bile duct) (LIRIb) for 15 min. The animals were killed 90 min, 5 h, and 24 h after reperfusion. Intact and sham operated rats served as controls. As indicated by semiquantitative estimation, increases in the number of Fos-positive cells mainly occurred 90 min after both liver reperfusion injuries, including activation of AVP and OXY perikarya in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, and TH, NPY, and PNMT perikarya in the catecholaminergic ventrolateral medullar A1/C1 area. Moreover, only PNMT perikarya located in the A1/C1 cell group exhibited increased Fos expression 5 h after LIRIb reperfusion. No or very low Fos expression was found 24 h after reperfusion in neuronal phenotypes studied. Our results show that both models of the LIRI activate, almost by the same effectiveness, a number of different neuronal phenotypes which stimulation may be associated with a complex of physiological responses induced by (1) surgery (NPY, TH, PNMT), (2) hemodynamic changes (AVP, OXY, TH, PNMT), (3) inflammation evoked by ischemia and subsequent reperfusion (TH), and (4) glucoprivation induced by fasting (NPY, PNMT, TH). All these events may contribute by different strength to the development of pathological alterations occurring during the liver ischemia–reperfusion injury.

Topics: Animals; Brain; Corticotropin-Releasing Hormone; Immunohistochemistry; Liver; Male; Neurons; Neuropeptide Y; Oxytocin; Phenotype; Phenylethanolamine N-Methyltransferase; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Reperfusion Injury; Tyrosine 3-Monooxygenase; Vasopressins

Recent studies show that oxytocin has various effects on cellular behaviors. Oxytocin is reported to stimulate cardiomyogenesis of embryonic stem cells and endothelial cell proliferation. Mesenchymal stem cells (MSCs) are widely used for cardiac repair, and we elucidated the effect of oxytocin on umbilical cord derived-MSCs (UCB-MSCs). UCB-MSCs were pretreated with oxytocin (100 nM) and washed with saline prior to experiments. To evaluate their angiogenic potential and migration activity, tube formation assay and Boyden chamber assay were performed. For in vivo study, ischemia-reperfusion was induced in rats, and UCB-MSCs with or without oxytocin pretreatment were injected into the infarcted myocardium to evaluate the engraftment of injected cells. Histological and hemodynamic studies were performed. Oxytocin-treated UCB-MSCs showed a decrease in tube formation but a drastic increase in transwell migration activity. The transcription level of matrix metalloproteinase (MMP)-2 was increased in oxytocin-treated UCB-MSCs. Knock-down of MMP-2 by use of siRNA restored the tube formation, while reducing transmigration activity. In rats injected with oxytocin-treated UCB-MSCs, cardiac fibrosis and CD68 infiltration in the peri-infarct zone were reduced, whereas cell engraftment and connexin43 expression were greater than in rats injected with untreated UCB-MSCs. By contrast, angiogenesis did not differ significantly between the two groups. Cardiac contractility was higher in the group injected with oxytocin-treated UCB-MSCs than in the group injected with phosphate-buffered saline alone. Collectively, oxytocin is an effective priming reagent for stem cells for application to damaged heart tissue.

Topics: Animals; Cell Movement; Cells, Cultured; Fetal Blood; Gene Knockdown Techniques; Male; Matrix Metalloproteinase 2; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; Oxytocin; Rats; Rats, Sprague-Dawley; Reperfusion Injury; RNA, Small Interfering

Various mechanisms have been proposed for the pathogenesis of postischemic hepatic injury, including the generation of reactive oxygen metabolites. Oxytocin (OT) possesses antisecretory, antiulcer effects, facilitates wound healing and has anti-inflammatory properties. Hepatic ischemia-reperfusion (I/R)-injury was induced by inflow occlusion to median and left liver lobes ( approximately 70%) for 30 min of ischemia followed by 1h reperfusion in female Sprague-Dawley rats under anesthesia. I/R group (n=8) was administered intraperitoneally either OT (500 microg/kg) or saline at 24 and 12 h before I/R and immediately before reperfusion. Sham-operated group that underwent laparotomy without hepatic ischemia served as the control. Rats were decapitated at the end of reperfusion period. Hepatic samples were obtained for the measurement of myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH) and collagen levels and histopathological analysis. Tumor necrosis factor-alfa (TNF-alpha) and transaminases (SGOT, SGPT) were assayed in serum samples. I/R injury caused significant increases in hepatic microscopic damage scores, MPO activity, collagen levels, transaminase, serum TNF-alpha levels. Oxytocin treatment significantly reversed the I/R-induced elevations in serum transaminase and TNF-alpha levels and in hepatic MPO and collagen levels, and reduced the hepatic damage scores. OT treatment had tendency to abolish I/R-induced increase in MDA levels, while GSH levels were not altered. These results suggest that OT has a protective role in hepatic I/R injury and its protective effect in the liver appears to be dependent on its inhibitory effect on neutrophil infiltration.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Collagen; Female; Fibrosis; Glutathione; Liver; Malondialdehyde; Neutrophil Infiltration; Oxytocin; Peroxidase; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Tumor Necrosis Factor-alpha

Oxytocin was previously shown to have anti-inflammatory effects in different inflammation models. The major objective of the present study was to evaluate the protective role of oxytocin (OT) in protecting the kidney against ischemia/reperfusion (I/R) injury.. Male Wistar albino rats (250-300 g) were unilaterally nephrectomized, and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. OT (1 mg/kg, ip) or vehicle was administered 15 min prior to ischemia and was repeated immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Creatinine and urea concentrations in blood were measured for the evaluation of renal function, while TNF-alpha and lactate dehydrogenase (LDH) levels were determined to evaluate generalized tissue damage. Formation of reactive oxygen species in renal tissue samples was monitored by chemiluminescence technique using luminol and lucigenin probes.. The results revealed that I/R injury increased (p<0.01-0.001) serum urea, creatinine, TNF-alpha and LDH levels, as well as MDA, MPO and reactive oxygen radical levels in the renal tissue, while decreasing renal GSH content. However, alterations in these biochemical and histopathological indices due to I/R injury were attenuated by OT treatment (p<0.05-0.001).. Since OT administration improved renal function and microscopic damage, along with the alleviation of oxidant tissue responses, it appears that oxytocin protects renal tissue against I/R-induced oxidative damage.

Topics: Animals; Creatinine; Disease Models, Animal; Glutathione; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Male; Malondialdehyde; Oxytocin; Peroxidase; Protective Agents; Rats; Rats, Wistar; Reactive Oxygen Species; Reperfusion Injury; Tumor Necrosis Factor-alpha; Urea