Testicular Ischemia-reperfusion Injury Research Articles

Effects of Titanium Dioxide Nanoparticles and Coenzyme Q10 on Testicular Ischemia-Reperfusion Injury: Role of the Mitochondrial Apoptosis Pathway

Background: Testicular ischemia-reperfusion (I/R) injury is a urological emergency that can lead to male infertility. So far, no suitable treatment has been found for it. Therefore, in the present study, we investigate the therapeutic effects of concomitant administration of coenzyme Q10 (CoQ10) and titanium dioxide nanoparticles (TiO2-NPs) on testicular I/R damage in rats and the expressions of genes involved in mitochondrial apoptosis, miR-21, and circRNA0001518. Materials and Methods: In this study, after induction of testicular torsion/detorsion, CoQ10 and TiO2-NPs were administered to the rats for ten days. Then, sperm extracted from the epididymides were analyzed for concentration, viability, morphology, and motility. The amount of apoptosis in testicular cells was studied by flow cytometry. Also, the expressions of the Bax and Bcl-2 genes, as well as miR-21 and circRNA0001518 levels were evaluated. Results: Sperm parameters improved in the rats’ testicular that received CoQ10. Administration of TiO2-NPs to healthy rats increased apoptosis and the Bax/Bcl-2 expression ratio. However, its administration to testicular I/R rats alone or in combination with CoQ10 caused a decrease in apoptosis, the Bax/Bcl-2 expression ratio, and an increase in miR-21 and circRNA0001518 expressions. Conclusion: Overall, individual or joint administration of TiO2-NPs or CoQ10 can have therapeutic effects on testicular I/R by altering the expressions of genes in the mitochondrial apoptotic pathway and their regulatory elements.

Vanillic acid attenuates testicular ischemia/reperfusion injury in rats

BackgroundTesticular torsion is an important pediatric problem and ischemia/reperfusion injury (IRI) is involved in its etiopathogenesis. Vanillic acid (VA) is a phenolic acid has strong antioxidant properties. To our knowledge, the ability of VA to reduce testicular IRI has not been previously investigated. It was therefore aimed to evaluate whether VA had a beneficial effect against testicular IRI model in rats for the first time. Twenty-four rats were segregated into four groups: sham control, torsion/detorsion (T/D), T/D + VA (50 mg/kg and 100 mg/kg). The levels of testicular oxidative stress, inflammation, endoplasmic reticulum (ER) stress and apoptosis markers were determined using colorimetric methods. Hematoxylin–eosin staining method was used in the histopathological evaluation.ResultsOxidative stress, inflammation, ER stress and apoptosis levels were significantly higher in testicular tissues of rats with only IRI model (p < 0.05). VA applications improved these injuries in a dose-dependent manner (p < 0.05). Moreover, it was found that the results of histological examinations supported the biochemical results to a statistically significant extent.ConclusionsIt was revealed that VA application can remove testicular IRI for the first time. This testicular protective efficacy of VA needs to be supported by more extensive preclinical studies.

Role of antioxidants in preventing testicular ischemia‑reperfusion injury: a narrative review.

Testicular ischemia-reperfusion injury (TIR) is a urological emergency common among male newborns, children, and adolescents. Testicular injury and its consequences, such as altered hormone production, subfertility, and infertility, are determined by the duration and degree of testicular torsion. Early diagnosis and treatment are crucial to preserving the testes and fertility. Previous studies suggest that reactive oxygen species contribute to the pathogenesis of TIR injury, but the underlying mechanism remains unclear. Several drugs/plants reportedly exhibit antioxidative activities to protect against TIR. This review summarizes current studies on the role of antioxidants in preventing experimental TIR injury and discusses the underlying pathophysiological mechanisms.

Evaluation of testicular torsion management in Ogbomoso, South-Western Nigeria and surgical detorsion-augmented treatment with phytochemical fractions of Corchorus olitorius leaf in experimental rats

BackgroundThere is need to investigate whether phytochemicals along with surgical detorsion could serve as better managements options in TT patients rather than surgical detorsion (SD) alone. MethodsThe descriptive cross-sectional part of this study is questionnaire-based addressing sociodemographic characteristics of participants and their experience in management of TT. In the experimental part, male rats (n = 32) were grouped into: sham, Ischemia-reperfusion injury (IRI), dichloromethane (DCM) and ethanol fraction (100 mg/kg) of CO. Evaluation of tissue GPx, total thiol, SOD, MDA and H2O2 was done. Serum estimations of nitrite, TNF-α and IL-6, MPO, sperm motility, count and viability was also carried out. Tissue expression of bax and caspase 3 was assessed. Results68.9 % respondents agreed that SD alone is non-effective in the management of TT while 83.6 % reported a need to augment surgery with medications. Oxidative stress markers like H2O2, MDA and nitrite increased by IRI were decreased in post-treatment groups, along with a significant increase in the tissue level of GSH, GST, SOD, GPx, and total thiol. Inflammatory mediators were elevated in IRI while post-treatment rats showed significant decrease. IRI decreased sperm count significantly this was reversed by post-treatment. Bax and caspase 3 was increased in IRI rats and post-treatment with CO fractions reduced them. ConclusionsQuantitative cross-sectional study has revealed through experience of clinicians that surgical detorsion alone is not effective in managing TT. Augmented treatment with CO leaf fractions suppressed testicular IRI through inhibition of pro-apoptotic proteins expression, oxidative stress and inflammation.

Baicalein Alleviates Testicular Ischemia-Reperfusion Injury in a Rat Model of Testicular Torsion-Detorsion.

Testicular torsion/detorsion-induced ischemia/reperfusion injury is partly due to the overgeneration of reactive oxygen species. Baicalein, a main bioactive constituent derived from the dried root of Scutellaria baicalensis Georgi, possesses powerful antioxidative and anti-inflammatory properties. Therefore, we designed the research to explore the possible protective effect of baicalein against testicular ischemia-reperfusion injury. Sprague-Dawley rats were randomized into 4 groups, including control, testicular ischemia-reperfusion, testicular ischemia-reperfusion+vehicle injection, and testicular ischemia-reperfusion+baicalein therapy groups. The control group received surgical exposure of the left testis without torsion-detorsion. In the testicular ischemia-reperfusion group, the left testis underwent 720° counterclockwise torsion for two hours and then was allowed detorsion. Rats in the testicular ischemia-reperfusion+vehicle injection group received intraperitoneal injection of the vehicle at detorsion. In the baicalein-treated group, the intraperitoneal administration of baicalein dissolved in the vehicle was performed at detorsion. At four hours or three months following testicular detorsion, testicular tissues were removed to detect the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) which can recruit neutrophils into the testis, myeloperoxidase activity (an index of neutrophil infiltration in the testis), protein expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in neutrophils which can catalyze reactive oxygen species production, malondialdehyde concentration (a common marker of reactive oxygen species), and spermatogenesis. Both testicular ischemia-reperfusion and testicular ischemia-reperfusion+vehicle injection significantly increased the TNF-α and IL-1β levels, myeloperoxidase activity, NADPH oxidase protein expression, and malondialdehyde concentration, while decreased spermatogenesis in ipsilateral testes. In contrast, baicalein administration remarkably reduced TNF-α and IL-1β levels, myeloperoxidase activity, NADPH oxidase protein expression, and malondialdehyde concentration and also elevated spermatogenesis in ipsilateral testes. The results of our experiment demonstrate that baicalein alleviates testicular ischemia-reperfusion injury by inhibiting TNF-α and IL-1β secretion, neutrophil infiltration in the testis, and NADPH oxidase protein expression in neutrophils to reduce reactive oxygen species production.

NOX-activated NLRP3 Inflammasome Pathway Triggers Pyroptosis During Testicular Ischemia Reperfusion Injury

NOX-activated NLRP3 Inflammasome Pathway Triggers Pyroptosis During Testicular Ischemia Reperfusion Injury

Targeting soluble guanylate cyclase with Riociguat has potency to alleviate testicular ischaemia reperfusion injury via regulating various cellular pathways.

Testicular ischaemia reperfusion (I/R) injury results with serious dysfunctions in testis. This study aims to explore effects of soluble guanylate cyclase (sGC) stimulator Riociguat on experimental testicular I/R injury in rats. Twenty-one male rats were divided into three groups (Control, IR and IRR). The control group was not exposed to any application. Bilateral testis from IR and IRR animals were rotated 720° in opposite directions for 3 h to induce experimental testicular ischaemia. Animals in IR and IRR groups were subjected to 3 h of reperfusion. Isotonic and Riociguat were administered to the animals 30 min prior reperfusion by oral gavage. At the end of experiment, animals were sacrificed and tissue samples were used for analyses. Riociguat treatment significantly decreased tissue malondialdehyde and Luminol levels compared to the IR group (p < 0.05). The pathological changes, pro-apoptotic proteins (Bax, Caspase 3, and Caspase 9) and apoptotic index in the IR group were down regulated in Riociguat treated animals (p < 0.05). Riociguat treatment was also significantly increased anti-apoptotic Bcl-2 expression, but alleviated tissue injury via modulating pro-inflammatory cytokine IL-1β levels and significantly (p < 0.05) down-regulating NF-κB activity. Moreover, mTOR and ERK phosphorylation increased in IR group (p < 0.05), but Riociguat treatment reduced protein phosphorylation. Our experiment indicated that targeting sGC might support surgical interventions in testicular I/R injury by modulating oxidative stress, inflammation, and apoptotic protein expression levels, but more detailed studies are required to explore the protective activity of Riociguat and underlying mechanisms in testicular I/R injury.

Salidroside Exerts Beneficial Effect on Testicular Ischemia-Reperfusion Injury in Rats

Testicular torsion-detorsion results in testicular ischemia-reperfusion injury, which is associated with overgeneration of reactive oxygen species. Salidroside, a major bioactive ingredient extracted from Rhodiola rosea, has strong antioxidant activity. The purpose of this study was to examine the effect of salidroside on testicular ischemia-reperfusion injury. Sixty rats were randomly separated into 3 experimental groups: group A = sham-operated control; group B = testicular ischemia-reperfusion; and group C = testicular ischemia-reperfusion treated with salidroside. The rats in the sham-operated control group received all surgical procedures except testicular torsion-detorsion. The testicular ischemia-reperfusion group underwent 2 hours of left testicular torsion followed by detorsion. The rats in the salidroside-treated group received the same surgical procedure as in testicular ischemia-reperfusion group, but salidroside was injected intraperitoneally at reperfusion. Testicular malondialdehyde content (a reliable index of reactive oxygen species) and protein expression of superoxide dismutase and catalase which are primary antioxidant enzymes in testes were measured at 4 hours after reperfusion. Testicular spermatogenesis was evaluated at 3 months after reperfusion. The malondialdehyde content increased significantly, while superoxide dismutase and catalase protein expression and testicular spermatogenesis reduced significantly in ipsilateral testes of testicular ischemia-reperfusion group, as compared with sham-operated control group. Therapy with salidroside significantly reduced malondialdehyde content and significantly enhanced superoxide dismutase and catalase protein expression and spermatogenesis in ipsilateral testes, as compared with testicular ischemia-reperfusion group. The present findings indicate that treatment with salidroside ameliorates testicular ischemia-reperfusion injury by reducing reactive oxygen species level by upregulating superoxide dismutase and catalase protein expression.

Pathological analysis of spermatic dysfunction in testicular ischemia-reperfusion injury

ABSTRACT Introduction &amp; Objectives Testicular ischemia represented by torsion needs emergency surgery to reperfuse testicular blood flow. However, spermatic dysfunction is often led despite appropriate treatment. Pathology of spermatic dysfunction following testicular ischemia-reperfusion injury (IRI) is still unclear. In previous research, Inflammation and excessive oxidative stress were thought to be involved in tissue dysfunction following IRI. We hypothesized that inflammation and excessive oxidative stress plays key role in spermatic dysfunction following testicular IRI. We investigated relevance between Inflammation / excessive oxidative stress and spermatic dysfunction using testicular IRI model mice. Materials &amp; Methods Ten to fifteen weeks old, C57BL/6 male were used through the study. Unilateral (left side) testicular vessels were clamped and de-clamped 1 hour later. Testicular blood flow was resumed. Sham operation mice were set as control. Bilateral testes were removed at 0(during ischemia), 1, 3, 5 weeks after modeling testicular IRI mice. Inflammation and oxidative stress changes in bilateral testis were investigated using histological, biochemical and immunohistochemical analysis. Spermatic changes extracted from the epididymal cauda were investigated using computer aided sperm analysis (CASA). Results Histological analysis using HE and Masson-Trichrome (MT) stain showed invasion of inflammatory cells and destruction of tissue structure from week 1. Inflammatory analysis using comprehensive protein assay and immunofluorescent stain showed increased expression of cytokines (IL-2, IL-3, IL-17A, IL-23), chemokines (CCL2, CCL5, CXCL1, CX3CL1), testes were showed from week1. Oxidative stress and cell death analysis using representative candidates (8-OHdG, ROS) showed increased expression of representative candidates from week0. Spermatic analysis showed that obvious decreased spermatic concentration and motility were showed from week 1. In contralateral testes, slow decreased spermatic concentration and motility was showed from week 1. Conclusions Spermatic dysfunction following testicular-ischemia reperfusion injury was induced in inflammatory and excessive oxidative stress changes. Inflammatory and excessive oxidative stress changes might be a novel regulatory factor for spermatic dysfunction following testicular ischemia-reperfusion injury. Disclosure Work supported by industry: no.

Astaxanthin Relieves Testicular Ischemia-Reperfusion Injury-Immunohistochemical and Biochemical Analyses.

Testicular torsion potentially leads to acute scrotum and testicle loss, and requires prompt surgical intervention to restore testicular blood flow, despite the paradoxical negative effect of reperfusion. While no drug is yet approved for this condition, antioxidants are promising candidates. This study aimed to determine astaxanthin’s (ASX), a potent antioxidant, effect on rat testicular torsion−detorsion injury. Thirty-two prepubertal male Fischer rats were divided into four groups. Group 1 underwent sham surgery. In group 2, the right testis was twisted at 720° for 90 min. After 90 min of reperfusion, the testis was removed. ASX was administered intraperitoneally at the time of detorsion (group 3) and 45 min after detorsion (group 4). Quantification of caspase-3 positive cells and oxidative stress markers detection were determined immunohistochemically, while the malondialdehyde (MDA) value, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were determined by colorimetric assays. The number of apoptotic caspase-3 positive cells and the MDA value were lower in group 4 compared to group 2. A significant increase in the SOD and GPx activity was observed in group 4 compared to groups 2 and 3. We conclude that ASX has a favorable effect on testicular ischemia-reperfusion injury in rats.

Attenuation Effect of Salvianolic Acid B on Testicular Ischemia-Reperfusion Injury in Rats.

During testicular ischemia-reperfusion, overproduction of reactive oxygen species is associated with testicular injury. We injected hydrogen peroxide (a representative of reactive oxygen species) into normal testis via the testicular artery. The experiment demonstrates that reactive oxygen species can cause spermatogenic injury. Salvianolic acid B, the most abundant bioactive component in Salvia miltiorrhiza Bunge, has been reported to possess a potent antioxidant activity. This study was conducted to evaluate the effect of salvianolic acid B on testicular ischemia-reperfusion injury in a rat testicular torsion-detorsion model. Rats were randomly separated into three groups, including 20 rats in each group: control group with sham operation, testicular ischemia-reperfusion group, and testicular ischemia-reperfusion + salvianolic acid B-treated group. In the testicular ischemia-reperfusion group, left testicular torsion of 720° for 2 hours was induced, and then testicular detorsion was carried out. Rats in the salvianolic acid B-treated group additionally had salvianolic acid B administered intravenously at detorsion. At 4 hours after detorsion, testes of 10 rats from each group were collected to analyze the protein expression of xanthine oxidase which catalyzes generation of reactive oxygen species and malondialdehyde concentration (an indirect indicator of reactive oxygen species). At 3 months after detorsion, testes of the remaining 10 rats from each group were collected to analyze spermatogenesis. Compared with the control group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes of testicular ischemia-reperfusion group increased significantly, while spermatogenesis decreased significantly. In the salvianolic acid B-treated group, xanthine oxidase protein expression and malondialdehyde concentration in ipsilateral testes decreased significantly, while spermatogenesis increased significantly, compared with the testicular ischemia-reperfusion group. These results suggest that salvianolic acid B can attenuate testicular torsion/detorsion-induced ischemia/reperfusion injury by downregulating the xanthine oxidase protein expression to inhibit reactive oxygen species formation.

The effects of etomidate on testicular ischemia reperfusion injury in ipsilateral and contralateral testes of rats.

Testicular torsion is a condition that manifests with acute pain and can lead to infertility despite urgent surgical intervention. The aim of this study is to investigate the protective and preventive effects of etomidate, an imidazole derivative, a non-barbiturate general anesthetic agent, without analgesic effect, on testicular ischemia-reperfusion injury. Twenty-four adult male Wistar rats weighing 200-250 g were used in the study. Torsion was created in all rats by rotating left testes 720° clockwise on the day of the experiment. 30 minutes before detorsion, 4 mg/kg etomidate and 10 mg/kg propofol were administered intraperitoneally to the etomidate and propofol groups, respectively. After an hour of ischemia, the left testis was reinstated, and the tissues were repaired according to their physiology. Following 24 hours of reperfusion, the animals were euthanized after ipsilateral and contralateral testes were removed. Etomidate applied before testicular detorsion significantly suppressed germ cell damage and Leydig cell loss in ipsilateral tissue. It did not cause any significant changes in the percentage of necrosis, histological score, and tubule rupture in ipsilateral tissue. Propofol administered before testicular detorsion significantly suppressed the percentage of necrosis only in the ipsilateral tissue. In addition, no signs of damage were observed in the contralateral testis. These findings show that etomidate administered before detortion creates a protective effect by preventing testicular ischemia-reperfusion injury.

Long-term protective effect of tadalafil on spermatogenesis following testicular ischemia-reperfusion injury in a rat model

Background: Testicular torsion is a urologic emergency that can lead to testicular atrophy and infertility owing to ischemia-reperfusion injury (IRI). The aim of this study was to evaluate the long-term protective effect of tadalafil, a phosphodiesterase-5 inhibitor used to treat erectile dysfunction, on spermatogenesis in a rat testicular model of IRI. Methods: Forty-eight adolescent Sprague–Dawley rats were divided into six groups of 8 each (A–F). Sham operation was performed on group A. Group B underwent surgical 720∘ torsion of the left testis without any medication. Groups C, D, E and F underwent surgical torsion and administration of tadalafil at varying doses (0.3 and 1.0 mg/kg) and durations (single or daily administration for four weeks). After three hours of torsion, detorsion was performed on all groups except group A. Four weeks after the operation, both testes were evaluated for spermatogenesis using the Johnsen scoring system. To evaluate the protective effect of tadalafil against oxidative stress induced by IRI, the malondialdehyde and superoxide dismutase levels of both testes were analyzed four hours after detorsion using the same experimental protocol as for groups A, B, and C. Results: Experimental groups treated with high-dose tadalafil showed higher Johnsen scores for spermatogenesis than the low-dose groups. Groups that received daily tadalafil administration for four weeks showed higher Johnsen scores than those receiving single doses. Furthermore, histopathologic findings and molecular markers related to oxidative stress were markedly improved following tadalafil administration. Conclusions: Tadalafil alleviated the oxidative stress and long-term deterioration of spermatogenesis in a rat testicular model of IRI by restoring the antioxidant status.

A Histological and Biochemical Study of The Protective Role of Hesperidin in Testicular Ischemia-Reperfusion Injury

A Histological and Biochemical Study of The Protective Role of Hesperidin in Testicular Ischemia-Reperfusion Injury

Idebenone regulates sirt1/Nrf2/TNF-α pathway with inhibition of oxidative stress, inflammation, and apoptosis in testicular torsion/detorsion in juvenile rats.

Testicular torsion is an emergency, mainly in newborn and adolescent males, resulting in testicular ischemia. The current study aimed to evaluate the effect of Idebenone (IDE) on testicular torsion/detorsion (T/D) in juvenile rats. Thirty-two rats were randomized into: (1) the sham group: rats received sham operations with no other interventions; (2) the IDE group: rats received idebenone (100mg/kg, i. p) without T/D; (3) the T/D group: rats underwent torsion for 2h and detorsion for 4h; and (4) the IDE+ T/D group: rats received IDE 1h before T/D. Testicular malondialdehyde (MDA), total nitrite/nitrate (NOx), total antioxidant capacity (TAC), tumor necrosis factor-α (TNF-α), caspase-3, sirtuin type 1 (Sirt1), serum interleukin-1β (IL-1β), total cholesterol, and testosterone were measured. Histological changes, nuclear factor (erythroid-derived 2)-like-2 factors (Nrf2), and proliferating cell nuclear antigen (PCNA) immuno-expressions were assessed. T/D displayed an increase in MDA, NOx, TNF-α, caspase-3, IL-1β, and total cholesterol with a significant decrease in TAC, Sirt1, and testosterone and strong positive Nrf2 and negative PCNA immuno-expressions. IDE could improve all oxidative, inflammatory, and apoptotic indicators. Therefore, IDE significantly reduced testicular ischemia-reperfusion injury in the juvenile rat testicular T/D model by limiting oxidative stress, inflammation, and apoptosis via the Sirt1/Nrf2/TNF-α pathway.

JAK Inhibition Prevents DNA Damage and Apoptosis in Testicular Ischemia-Reperfusion Injury via Modulation of the ATM/ATR/Chk Pathway.

Testicular ischemia reperfusion injury (tIRI) causes oxidative stress-induced DNA damage leading to germ cell apoptosis (GCA). The aim of the study is to establish a direct link between JAK2 activation and the DNA damage response (DDR) signaling pathways and their role in tIRI-induced GCA using AG490, a JAK2 specific inhibitor. Male Sprague Dawley rats (n = 36) were divided into three groups: sham, unilateral tIRI and tIRI + AG490 (40 mg/kg). During tIRI, augmentation in the phosphorylation levels of the JAK2/STAT1/STAT3 was measured by immunohistochemistry. Observed spermatogenic arrest was explained by the presence of considerable levels of DSB, AP sites and 8OHdG and activation of caspase 9, caspase 3 and PARP, which were measured by colorimetric assays and TUNEL. The ATM/Chk2/H2AX and ATR/Chk1 pathways were also activated as judged by their increased phosphorylation using Western blot. These observations were all prevented by AG490 inhibition of JAK2 activity. Our findings demonstrate that JAK2 regulates tIRI-induced GCA, oxidative DNA damage and activation of the ATM/Chk2/H2AX and ATR/Chk1 DDR pathways, but the cell made the apoptosis decision despite DDR efforts.

The Effects of Fentanyl on Testicular Ischemia-Reperfusion Injury.

Testicular torsion is a condition that often occurs as a result of the rotation of the spermatic cord in childhood and adolescence in men, manifests with acute pain and causes infertility in the future even if emergency intervention is performed. The aim of this study is to investigate the protective and preventive effects of fentanyl, a potent analgesic agent frequently used in anaesthesia practice, on testicular ischemia reperfusion injury, which manifests through acute pain. A total of 16 adult male Wistar rats, weighing 200-250 g, were used in this study. They were divided into two groups, consisting of eight animals in each group. Torsion was created in all rats by rotating left testicles 720 clockwise on the day of the experiment. 3 mM of fentanyl was applied intraperitoneally 30 minutes before detorsion to the fentanyl group. Following an hour of ischemia, the left testicle was reinstated, and tissues were repaired according to their physiology. Following 24 hours of reperfusion, the animals were euthanised after taking left testes and blood samples. Fentanyl, administered prior to testicular detorsion, significantly suppressed germ cell damage in torsioned tissue, catalase activity and malondialdehyde levels in blood samples taken from the heart. No significant differences were observed in plasma total thiol concentration, histological score, Leydig cell counts, percentage of necrosis and tubule rupture. These findings show that fentanyl administered before detortion creates a protective effect by preventing testicular ischemia reperfusion injury leading to infertility in the future.

Carvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia-reperfusion injury model.

Testicular torsion is a urological problem that causes subfertility and testicular damage in males. Testis torsion and detorsion lead to ischemia–reperfusion (IR) injury in the testis. Testicular IR injury causes the increase of reactive oxygen species (ROS), oxidative stress (OS) and germ cell-specific apoptosis. In this study, we aimed to investigate whether Carvacrol has a protective effect on testicular IR injury and its effects on Kir6.2 channels, which is a member of adenosine triphosphate (ATP)-dependent potassium channels. In the study, 2–4 months old 36 albino Wistar rats were used. For experimental testicular IR model, the left testis was rotated counterclockwise at 720° for two hours, and after two hours following torsion, detorsion was performed. Carvacrol was dissolved in 5% Dimethyl Sulfoxide (DMSO) at a dose of 73 mg/kg and half an hour before detorsion, 0.2 mL was administered intraperitoneally. In testicular tissues, caspase 3 and Kir6.2 immunoexpressions were examined. Serum malondialdehyde (MDA) and testosterone levels were measured. Apoptotic cells and serum MDA levels were significantly decreased and Kir6.2 activation was significantly increased in Carvacrol-administrated IR group. As a result of our study, Carvacrol may activates Kir6.2 channels and inhibits apoptosis and may have a protective effect on testicular IR injury.

Remote limb ischaemic conditioning produces cardioprotection in rats with testicular ischaemia-reperfusion injury.

What is the central question of this study? Can remote limb ischaemic conditioning produce cardioprotection in rats with testicular ischaemia-reperfusion injury? What is the main finding and its importance? Testicular ischaemia-reperfusion (TI/R)-injured rats were predisposed to myocardial reperfusion-induced atrioventricular block. Remote limb ischaemia preconditioning and postconditioning protected TI/R hearts against ischaemia-provoked ventricular arrhythmia and ultimately reduced the incidence of sudden cardiac death, with a possible role of c-Jun N-terminal kinase inhibition and connexin 43 activation. Remote ischaemic conditioning can protect hearts against arrhythmia. Testicularischaemia-reperfusion (TI/R) injury is associated with electrocardiographic abnormalities. We investigated the effect of remote limb ischaemia preconditioning (RIPre) and postconditioning (RIPost) on arrhythmogenesis in TI/R rats, and determined the potential role of c-Jun N-terminal kinase (JNK)/connexin 43 (Cx43) signalling. Rats were randomized to sham-operated, control, TI/R, RIPre and RIPost groups. TI/R rats were more predisposed to myocardial reperfusion-induced atrioventricular block (AVB). RIPre and RIPost reduced the incidence of sudden cardiac death (SCD) or AVB, and duration of ventricular tachyarrhythmias during myocardial reperfusion. RIPre and RIPost decreased myocardial I/R-induced phosphorylation level of JNK, while preserving myocardial Cx43 expression in TI/R rats. Taken together, TI/R rats were predisposed to myocardial reperfusion-induced AVB. RIPre and RIPost protected TI/R hearts against ischaemia-provoked ventricular arrhythmia and ultimately reduced the incidence of SCD by suppressing JNK activation and restoring Cx43 expression.

Relaxin exerts a protective effect during ischemia-reperfusion in the rat model.

Testicular torsion, which causes ischemia-reperfusion (IR) injury, is a serious urological emergency that can lead to testicular dysfunction, including infertility, primarily among newborn and pubertal males; thus, effective drugs should be administered during or after ischemia. Using a rat model of testicular IR injury, the present study investigated the protective effects of relaxin (RLN) against oxidative stress, testicular dysfunction, inflammation, histological damage, arrested spermatogenesis, and germ cell apoptosis as well as explored the usefulness of RLN as a potential protective drug for IR injury combined with surgical treatment. Male Sprague-Dawley rats were subjected to left testicular ischemia for 2 h, followed by 24 h of reperfusion. They were subsequently divided into three groups: sham, IR, and IR + RLN groups. Porcine RLN (500ng/h) or saline was infused using an implanted osmotic mini-pump 90min after inducing ischemia. The RLN dose used herein was that which resulted in serum RLN levels comparable to those in mid-pregnant rats based on previous studies. Testicular IR increased germ cell apoptosis and histological damage as well as promoted disorganized and arrested spermatogenesis, accompanied by a significant increase in oxidative stress and inflammation. However, RLN administration ameliorated the adverse consequences associated with IR injury by attenuating oxidative stress and mitigating apoptosis and inflammation. The study findings clearly demonstrated that RLN exerts a protective effect against IR-induced testicular injury by attenuating oxidative stress, apoptosis, and inflammation, suggesting that RLN together with surgical treatment is a potentially efficacious approach toward ameliorating testicular dysfunction following testicular torsion.