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The mechanism of PDE5 inhibitor. Sexual arousal causes enhanced level of NO, which stimulate the guanylyl cyclase to convert GTP to cGMP. PDE5 inhibitor, inhibit the PDE5 enzyme, which is responsible for the catabolism of cGMP to 5'-GMP. The increased level of cGMP activates the protein kinase G, which decreases the Ca 2+ level. As a result of this, smooth muscle relaxation and subsequently erection are formed.

The mechanism of PDE5 inhibitor. Sexual arousal causes enhanced level of NO, which stimulate the guanylyl cyclase to convert GTP to cGMP. PDE5 inhibitor, inhibit the PDE5 enzyme, which is responsible for the catabolism of cGMP to 5'-GMP. The increased level of cGMP activates the protein kinase G, which decreases the Ca 2+ level. As a result of this, smooth muscle relaxation and subsequently erection are formed.

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PurposeInvestigate the short-term effect of sildenafil on microcirculation, especially the velocity, the pattern of the flow and the recruitment of the leukocyte in postcapillaries. Methods In male Sprague–Dawley rats, the microcirculatory consequences of 60 min experimental testicular torsion, followed by 240 min of reperfusion, were examined. Usi...

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... our current study, we aimed to examine the effect of sildenafil (Figure 2.) on microcirculation by measuring the recruitment of the leukocyte and red blood cell velocity (RBCV), and the pattern of the flow in post-capillaries examined with IVM, before and after I/R damage in rat testicles. ...
Context 2
... our current study, we aimed to examine the effect of sildenafil (Figure 2.) on microcirculation by measuring the recruitment of the leukocyte and red blood cell velocity (RBCV), and the pattern of the flow in post-capillaries examined with IVM, before and after I/R damage in rat testicles. ...

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... Although reperfusion is vital to the persistence of ischemic tissue, it leads to other cellular damage [72]. After testicular detorsion, ROS formed in these tissue causing injuries in the testicular lipids, proteins, carbohydrates and DNA, which leads to germinal cell apoptosis [73]. GPx is one of the antioxidant enzymes that aids in the conversion of ROS into less reactive species. ...
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Testicular torsion (TT) is the most common urological emergency in children and young adults that can lead to infertility in many cases. The ischemia-reperfusion (IR) injury due to TT has been implicated in the pathogenesis of testicular damage. The main pathological mechanisms of contralateral injury after ipsilateral TT are not fully understood. In the presented study, we investigated the molecular and microscopic basis of ipsilateral and contralateral testicular injury following ipsilateral testicular torsion detorsion (T/D) and explored the possible protective role of vitamin D3. The biochemical analysis indicated that IR injury following T/D significantly decreased the activity of testicular glutathione peroxidase (GPx) enzyme, level of serum testosterone, serum inhibin B, and expression of testicular miRNA145, while increased the activity of testicular myeloperoxidase (MPO) enzyme, level of testicular malondialdehyde (MDA), level of serum antisperm-antibody (AsAb), and expression of ADAM-17. The histological and semen analysis revealed that torsion of the testis caused damages on different tissues in testis. Interestingly, administration of vitamin D3 prior to the IR injury reversed the deterioration effect of IR injury on the testicular tissues as indicated by biochemical and histological analysis which revealed normal appearance of the seminiferous tubules with an apparent decrease in collagen fiber deposition in both ipsilateral and contralateral testes. Our results revealed that the protective effect of vitamin D3 treatment could be attributed to target miRNA145 and ADAM17 protein. To further investigate these findings, we performed a detailed molecular modelling study in order to explore the binding affinity of vitamin D3 toward ADAM17 protein. Our results revealed that vitamin D3 has the ability to bind to the active site of ADAM17 protein via a set of hydrophobic and hydrophilic interactions with high docking score. In conclusion, this study highlights the protective pharmacological application of vitamin D3 to ameliorate the damages of testicular T/D on the testicular tissues via targeting miRNA145 and ADAM17 protein.
Article
Background: Semen quality impairment is a serious consequence of testicular torsion–detorsion (TD). Adequate germ-cell mitochondrial oxidative phosphorylation (OXPHOS) plays a crucial role in male fertility. Changes in cellular OXPHOS in testicular tissues after testicular TD remain unclear. Objectives: This study investigated whether testicular TD induces alternations of mitochondrial OXPHOS in testicular tissues. Materials and methods: BALB/c male mice were divided into a Sham group and a testicular TD group. At the end of the procedure, the mice were euthanized, and their bilateral testicles were removed. Mitochondria morphology was evaluated through transmission electron microscopy. The cellular respiratory functions of germ cells were evaluated using a Seahorse analyzer assay. The proteome profiles in testicular tissues were analyzed using liquid chromatography–tandem mass spectrometry (LC-MS/MS). The differences in the expression levels of each component in the OXPHOS were revealed using Ingenuity Pathways Analysis (IPA). Results: Inner mitochondrial membrane disruption was found in ipsilateral twisted testicular mitochondria in the TD group but not in contralateral untwisted testes. The cellular respiratory function in germ cells were significantly decreased after testicular TD in ipsilateral twisted testes but not in contralateral untwisted testes. LC-MS/MS analysis of ipsilateral twisted testicular tissue revealed that mitochondrial proteins were differentially expressed after testicular TD. Testicular TD induced downregulation of OXPHOS and revealed alternations of specific proteins in the OXPHOS complexes. Discussion and conclusion: Testicular TD produced mitochondria injury and dysregulation of mitochondrial OXPHOS in ipsilateral twisted testes. Different protein expressions were identified in the mitochondrial OXPHOS complexes with testicular TD; new therapeutic targets may be identified to restore the OXPHOS function of germ cells. This article is protected by copyright. All rights reserved