Effects of 3-aminobenzamide on unilateral testicular ischemia–reperfusion injury: What is the role of PARP inhibition?

The therapeutic effects of poly(adenosine diphosphate-ribose) polymerase inhibition by 3-aminobenzamide (3-AB) were investigated in testicular ischemia–reperfusion (I/R) injury, using sperm analysis and histopathological and biochemical examinations, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities and reduced glutathione (GSH) levels. Male rats were divided into 3 groups: sham (n = 12), I/R (n = 12), and I/R with 3-AB (I/R–3-AB) (n = 12). The left testicular artery was occluded for 1 h, followed by 24 h (for biochemical and histopathological examinations) and 30 days (for sperm analysis) of reperfusion. 3-AB treatment intraperitoneally 10 min prior to and 1 h after reperfusion increased the I/R-induced decrease in sperm motility in both testes and reduced the increased abnormal sperm rates in the ipsilateral testis. However, 3-AB treatment failed to prevent the I/R-induced decrease in sperm concentration in both testes. SOD and CAT activities did not change in any group. GSH-Px activity and GSH levels were increased by I/R. 3-AB treatment reversed the I/R-induced increase in GSH-Px activity, similar to the level in sham rats, but did not alter GSH levels. 3-AB treatment significantly increased the I/R-induced decrease in histopathologic score. In conclusion, 3-AB treatment has potential biochemical and histopathological benefits beyond improving sperm quality and may have the potential to decrease damage from testicular torsion.

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The Effect of Poly (Adenosine Diphosphate-Ribose) Polymerase Inhibitors on Biochemical Changes in Testicular Ischemia-Reperfusion Injury

The Journal of Urology ◽

10.1097/01.ju.0000049228.37887.4d ◽

2003 ◽

Vol 169 (5) ◽

pp. 1870-1873 ◽

Cited By ~ 31

Author(s):

MURAT BOZLU ◽

GÜLÇİN ESKANDARİ ◽

SELAHİTTİN ÇAYAN ◽

BÜLENT CANPOLAT ◽

ERDEM AKBAY ◽

...

Keyword(s):

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Adenosine Diphosphate ◽

Biochemical Changes ◽

Polymerase Inhibitors ◽

Testicular Ischemia

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Protective Effects of Topical Application of Nitrite on Testicular Ischemia-Reperfusion Injury in Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/5514537 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Jae Won Lee ◽

Ee Taek Hwang ◽

Jin Soo Han

Keyword(s):

Reperfusion Injury ◽

Topical Application ◽

Testicular Torsion ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Therapeutic Effects ◽

Treatment Groups ◽

Group A ◽

Testicular Ischemia ◽

Group B

Testicular torsion is a urologic emergency induced by torsion of the spermatic cord, interrupting blood circulation to the testis. Therapeutic options for testicular torsion, except surgical restoration of testis, are rarely applied in clinical practice. This study, therefore, investigated whether topical application of nitrite (NO2-) is beneficial in tissue damage due to testicular ischemia-reperfusion (I/R) injury in rats. Pubertal Sprague-Dawley rats were assigned to seven groups: group A, sham-operated control group; group B, I/R with no treatment; groups C, D, and E, I/R followed by treatment with three different doses of nitrite; group F, I/R followed by administration of nitrite and a NO scavenger, C-PTIO (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt); and group G, I/R followed by administration of nitrate (NO3-). Unilateral testicular ischemia was maintained for 5 h, followed by reperfusion for 24 h. Nitrite and nitrate were topically administered before reperfusion. Compared to group A, germ cell apoptosis, oxidative stress, antioxidant enzymatic function, and lipid peroxidation were significantly increased, along with abnormal morphology and impaired spermatogenesis in group B ( P < 0.05 ). In contrast, testicular damage was generally attenuated in the nitrite treatment groups due to a reduction in superoxide and peroxynitrite levels and the inhibition of caspase-3-dependent apoptosis ( P < 0.05 vs. group B). These therapeutic effects of nitrite-derived NO were suppressed after injection of C-PTIO, which showed in group F. Taken together, our results demonstrate that topical application of nitrite may be one of the therapeutic strategies for testicular ischemia-reperfusion injury.

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Melanocortin 4 Receptor Activation Protects Against Testicular Ischemia-Reperfusion Injury by Triggering the Cholinergic Antiinflammatory Pathway

Endocrinology ◽

10.1210/en.2011-1016 ◽

2011 ◽

Vol 152 (10) ◽

pp. 3852-3861 ◽

Cited By ~ 18

Author(s):

Letteria Minutoli ◽

Alessandra Bitto ◽

Francesco Squadrito ◽

Natasha Irrera ◽

Mariagrazia Rinaldi ◽

...

Keyword(s):

Vagus Nerve ◽

Receptor Antagonist ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Organ Damage ◽

Receptor Activation ◽

Male Rats ◽

Efferent Activity ◽

Tnf Α ◽

Testicular Ischemia

Melanocortins (MC) trigger a vagus nerve-mediated cholinergic-antiinflammatory pathway projecting to the testis. We tested whether pharmacological activation of brain MC receptors might protect the testis from the damage induced by ischemia-reperfusion. Adult male rats were subjected to 1-h testicular ischemia, followed by 24-h reperfusion [testicular ischemia-reperfusion (TI/R)]. Before TI/R, groups of animals were subjected to bilateral cervical vagotomy, or pretreated with the nicotinic acetylcholine receptor antagonist chlorisondamine or the selective MC4 receptor antagonist HS024. Immediately after reperfusion, rats were ip treated with saline or the MC analog [Nle4,D-Phe7]α-melanocyte-stimulating hormone (NDP-α-MSH) (340 μg/kg). We evaluated testicular IL-6 and TNF-α by Western blot analysis and organ damage by light microscopy. Some experimental groups were prepared for neural efferent activity recording along the vagus nerve starting 30 min after treatment with NDP-α-MSH or saline, and for a 30-min period. Additional groups of TI/R rats were treated for 30 d with saline, NDP-α-MSH, chlorisondamine plus NDP-α-MSH, or HS024 plus NDP-α-MSH to evaluate spermatogenesis, organ damage, and the apoptosis machinery. After a 24-h reperfusion, in TI/R saline-treated rats, there was an increase in IL-6 and TNF-α expression and a marked damage in both testes. NDP-α-MSH inhibited IL-6 and TNF-α expression, decreased histological damage, and increased neural efferent activity. Furthermore, NDP-α-MSH administration for 30 d greatly improved spermatogenesis, reduced organ damage, and inhibited apoptosis. All positive NDP-α-MSH effects were abrogated by vagotomy, chlorisondamine, or HS024. Our data suggest that selective MC4 receptor agonists might be therapeutic candidates for the management of testicular torsion.

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Beneficial Effect of Continuous Normobaric Hypoxia on Ventricular Dilatation in Rats With Post-Infarction Heart Failure

Physiological Research ◽

10.33549/physiolres.933308 ◽

2016 ◽

pp. 867-870 ◽

Cited By ~ 6

Author(s):

J. HRDLIČKA ◽

J. NECKÁŘ ◽

F. PAPOUŠEK ◽

J. VAŠINOVÁ ◽

P. ALÁNOVÁ ◽

...

Keyword(s):

Heart Failure ◽

Prolonged Exposure ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Coronary Artery Occlusion ◽

Normobaric Hypoxia ◽

Male Rats ◽

Ventricular Dilatation ◽

Sham Operation ◽

Therapeutic Effects

Adaptation to continuous normobaric hypoxia (CNH) protects the heart against ischemia/reperfusion injury but much less is known about its potential therapeutic effects. The aim of this study was to find out whether post-infarction exposure to CNH can attenuate the progression of heart failure. Ten-week-old male rats underwent myocardial infarction (MI) or sham operation. MI was induced by 60-min coronary artery occlusion. Seven days post-MI, the rats were randomly assigned to two groups: i) sedentary controls kept at room air and ii) rats exposed to CNH (12 % O2, 3 weeks). Echocardiographic examination of the left ventricle (LV) was performed 3 days before surgery and 7, 14 and 28 days post-MI. MI resulted in a gradual increase in LV end-diastolic diameter (LVDd) compared to sham-operated animals. Fractional shortening (FS) decreased from 42.8 % before MI to 15.1 % on day 28 post-MI. CNH significantly attenuated ventricular dilatation without affecting scar area and FS. Our data suggest that prolonged exposure to CNH has certain potential to attenuate the progression of unfavorable changes in ventricular geometry induced by MI in rats.

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Inhibition of poly(adenosine diphosphate-ribose) polymerase decreases long-term histologic damage in testicular ischemia-reperfusion injury

Urology ◽

10.1016/j.urology.2003.10.062 ◽

2004 ◽

Vol 63 (4) ◽

pp. 791-795 ◽

Cited By ~ 25

Author(s):

Murat Bozlu ◽

Banu Coşkun ◽

Selahİttİn Çayan ◽

Denİz Acar ◽

Savaş Aktaş ◽

...

Keyword(s):

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Adenosine Diphosphate ◽

Testicular Ischemia

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Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

10.36295/asro.2019.220415 ◽

2019 ◽

Vol 22 (04) ◽

pp. 122-130

Author(s):

Rihab H Al-Mudhaffer ◽

Laith M Abbas Al-Huseini ◽

Saif M Hassan ◽

Najah R Hadi

Keyword(s):

Cerebral Ischemia ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Male Rats ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury

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Propofol attenuates lung ischemia/reperfusion injury though the involvement of the MALAT1/microRNA-144/GSK3β axis

Molecular Medicine ◽

10.1186/s10020-021-00332-0 ◽

2021 ◽

Vol 27 (1) ◽

Author(s):

Jian-Ping Zhang ◽

Wei-Jing Zhang ◽

Miao Yang ◽

Hua Fang

Keyword(s):

Cell Apoptosis ◽

Ischemia Reperfusion Injury ◽

Glycogen Synthase ◽

Ischemia Reperfusion ◽

Inflammatory Factors ◽

Therapeutic Effects ◽

Protective Effects ◽

Loss Of Function

Abstract Background Propofol, an intravenous anesthetic, was proven to protect against lung ischemia/reperfusion (I/R) injury. However, the detailed mechanism of Propofol in lung I/R injury is still elusive. This study was designed to explore the therapeutic effects of Propofol, both in vivo and in vitro, on lung I/R injury and the underlying mechanisms related to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-144 (miR-144)/glycogen synthase kinase-3β (GSK3β). Methods C57BL/6 mice were used to establish a lung I/R injury model while pulmonary microvascular endothelial cells (PMVECs) were constructed as hypoxia/reperfusion (H/R) cellular model, both of which were performed with Propofol treatment. Gain- or loss-of-function approaches were subsequently employed, followed by observation of cell apoptosis in lung tissues and evaluation of proliferative and apoptotic capabilities in H/R cells. Meanwhile, the inflammatory factors, autophagosomes, and autophagy-related proteins were measured. Results Our experimental data revealed that Propofol treatment could decrease the elevated expression of MALAT1 following I/R injury or H/R induction, indicating its protection against lung I/R injury. Additionally, overexpressing MALAT1 or GSK3β promoted the activation of autophagosomes, proinflammatory factor release, and cell apoptosis, suggesting that overexpressing MALAT1 or GSK3β may reverse the protective effects of Propofol against lung I/R injury. MALAT1 was identified to negatively regulate miR-144 to upregulate the GSK3β expression. Conclusion Overall, our study demonstrated that Propofol played a protective role in lung I/R injury by suppressing autophagy and decreasing release of inflammatory factors, with the possible involvement of the MALAT1/miR-144/GSK3β axis.

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