Protective effect of pterostilbene on testicular ischemia/reperfusion injury in rats

Kim, Hyung Joon; Lee, Jae Won; Hwang, Bo Ram; Lee, Young Ah; Kim, Jong-In; Cho, Yoon Ju; Jhun, Hyun Jhung; Han, Jin Soo

doi:10.1016/j.jpedsurg.2016.01.009

Cited by 15 publications

(11 citation statements)

References 20 publications

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“…Oxidative stress and lipid peroxidation are considered to be fatal contributors to the pathophysiological process of testicular I/R injury (2). In the testes, lipid peroxidation results in oxidative damage and cytotoxicity to germ cells and Sertoli cells, inducing massive apoptosis-mediated germ cell death (2,19,29,(46)(47)(48). considering the yet-uncharacterized role of I/R injury-induced lipid peroxidation in Sertoli cell death, the modality of TM4 cell death was investigated.…”

Section: Discussionmentioning

confidence: 99%

“…Testicular I/R injury has been reported to induce cell death in germ cells, but not in Sertoli cells (19,28,29). It was therefore examined whether I/R was able to induce cell death in Sertoli cells.…”

Section: Ferroptosis Is Induced Following I/r Injury In Tm4 Cellsmentioning

confidence: 99%

“…Germ cell loss following testicular I/R injury may result in part from Sertoli cell damage-dependent alterations in the microenvironment (16)(17)(18). The mechanism of testicular I/R injury is lipid peroxidation (19). Previous studies have reported that I/R induces ferroptosis in nephritic tubular cells and hepatocytes, whereas other forms of regulated cell death are not observed (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

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Ferroptosis is associated with oxygen-glucose deprivation/reoxygenation-induced Sertoli cell death

Zhao

et al. 2018

Int J Mol Med

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Sertoli cell death contributes to spermatogenesis impairment, which is associated with male infertility. Testicular ischemia‑reperfusion (I/R) injury induces the cell death of germ cells and Sertoli cells, whereas inhibition of cell death ameliorates acute testicular I/R damage. The aim of the present study was to investigate the mechanism of I/R stress-induced cell death in TM4 cells. Oxygen‑glucose deprivation and reoxygenation (OGD/R) was demonstrated to induce I/R injury and cell death in TM4 cells. Cell death was blocked by the reactive oxygen species (ROS) inhibitor N‑acetylcysteine, as well as lipid peroxidation inhibitors Liproxstatin‑1 and iron chelator deferoxamine; however, inhibitors of apoptosis, necrosis or autophagy had no effect. It was also demonstrated that iron and lipid ROS levels were elevated in I/R injury and that mitochondria decreased in size and increased in membrane density, which is indicative of ferroptosis. Furthermore, the generation of lipid ROS suggests iron accumulation and glutathione (GSH) depletion. The expression of ferroportin (Fpn) protein and mRNA was decreased in TM4 cells. Notably, overexpression of Fpn inhibited ferroptosis, lipid ROS generation and iron accumulation. In addition, GSH‑dependent peroxidase 4 (GPX4) was inactivated via GSH depletion following I/R injury, whereas GPX4 activation blocked I/R‑induced ferroptosis by reducing lipid ROS levels. The mitogen‑activated protein kinase (MAPK) pathway was also investigated in the present study; it was observed that I/R‑induced ferroptosis was blocked by inhibiting p38 MAPK activation. The results of the present study demonstrate that ferroptosis is a pervasive and dynamic type of cell death induced by OGD/R injury in Sertoli cells. This may provide a novel insight into the application of cytoprotection in testicular I/R damage‑induced cell loss.

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Section: Discussionmentioning

confidence: 99%

Section: Ferroptosis Is Induced Following I/r Injury In Tm4 Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Ferroptosis is associated with oxygen-glucose deprivation/reoxygenation-induced Sertoli cell death

Zhao

et al. 2018

Int J Mol Med

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“…also observed that lutein treatment may prevent testicular IRI spermatogenic damage by interfering with its modulation of the survivor activating factor enhancement pathway (51). Pterostillbene (52), dexmedetomidine (53), curcumin (54), apocynin (55), 2-APB (56), interleukin-10 (57), tyrphostin AG 556 (58), desferrioxamine (59), and hyperbaric oxygen therapy (60) have all shown protective effect against testicular IRI at some capacity. Another possible novel therapeutic target for minimizing IRI that warrants further study is chemical histone deacetylase (HDAC) inhibitors, as Hou et al .…”

Section: Managementmentioning

confidence: 99%

Testicular compartment syndrome: an overview of pathophysiology, etiology, evaluation, and management

Gandhi

Dagur

Sheynkin

et al. 2016

Transl. Androl. Urol.

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Testicular compartment syndrome (TCS) refers to the impairment of microcirculation in the testicle due to either increased venous resistance or extraluminal compression, which leads to hypoxia. TCS releases oxidants through hypoxia and ischemia/reperfusion injury (IRI). The pathophysiology, etiology, evaluation, and management of TCS are reviewed. Based on the properties of TCS, specific causes, e.g., varicocele, hydrocele, orchitis, cryptorchidism, and scrotal hernia, are suggested and categorized. The oxidant-induced stress from TCS may explain the correlations between these causes and infertility. A chief shortcoming of current imaging modalities is that they detect TCS late after it has progressed to impair the macrocirculation of the testicle. We propose frequent sequential periodic power Doppler ultrasonography to monitoring for earlier detection. Intraoperatively, TCS can be diagnosed by the dull purple appearance of a hypoxic testicle and by tissue pressures above 30 mmHg. When compartment pressure is low, the underlying etiology must be promptly treated. During acute presentation, an incision of the resilient tunica albuginea may be necessary. A great challenge of treating TCS is restoring microcirculation while minimizing IRI; concomitant antioxidant therapy secondary to treatment may be effective and harmless at the least. Because testicular oxidant stress is common in infertility and since TCS can cause such a stress, TCS may be a larger factor in infertility than currently suspected.

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“…Since prolonged ischemia of the testis can lead to irreversible damage, prompt clinical treatment should be adopted to restore blood flow within an appropriate time frame [2, 3]. However, testicular detorsion can cause progressive reperfusion injury and its damage can be more serious than ischemic injury [4].…”

Section: Introductionmentioning

confidence: 99%

MALAT1 Promotes Cell Apoptosis and Suppresses Cell Proliferation in Testicular Ischemia-Reperfusion Injury by Sponging MiR-214 to Modulate TRPV4 Expression

Ning

Fang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Accumulating evidences has indicated that aberrant expression of long non-coding RNAs (lncRNAs) is tightly associated with the progression of ischemia-reperfusion injury (IRI). Previous studies have reported that lncRNA MALAT1 regulates cell apoptosis and proliferation in myocardial and cerebral IRI. However, the underlying mechanism of MALAT1 in testicular IRI has not been elucidated. Methods: The levels of MALAT1, some related proteins and apoptosis in the testicular tissues were determined by quantitative real-time PCR, HE staining, immunohistochemistry, western blot and TUNEL assays. Relative expression of MALAT1, miR-214 and related proteins in cells were measured by western blot and quantitative real-time PCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. Results: In the present study, we found that MALAT1 was up-regulated in animal samples and GC-1 cells. The expression level of MALAT1 was positively related to cell apoptosis and negatively correlated with cell proliferation as testicular IRI progressed. In gain and loss of function assays, we confirmed that MALAT1 promotes cell apoptosis and suppresses cell proliferation in vitro and in vivo. Furthermore, we found that MALAT1 negatively regulates expression of miR-214 and promotes TRPV4 expression at the post-transcriptional level. Consequently, we investigated the correlation between MALAT1 and miR-214 and identified miR-214 as a direct target of MALAT1. In addition, we found that TRPV4 acted as a target of miR-214. Over-expression of miR-214 efficiently abrogated the up-regulation of TRPV4 induced by MALAT1, suggesting that MALAT1 positively regulates the expression of TRPV4 by sponging miR-214. Conclusion: In sum, our study indicated that the lncRNA MALAT1 promotes cell apoptosis and suppresses cell proliferation in testicular IRI via miR-214 and TRPV4.

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Protective effect of pterostilbene on testicular ischemia/reperfusion injury in rats

Cited by 15 publications

References 20 publications

Ferroptosis is associated with oxygen-glucose deprivation/reoxygenation-induced Sertoli cell death

Ferroptosis is associated with oxygen-glucose deprivation/reoxygenation-induced Sertoli cell death

Testicular compartment syndrome: an overview of pathophysiology, etiology, evaluation, and management

MALAT1 Promotes Cell Apoptosis and Suppresses Cell Proliferation in Testicular Ischemia-Reperfusion Injury by Sponging MiR-214 to Modulate TRPV4 Expression

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