Hyperbaric Oxygen Therapy Suppresses Apoptosis and Promotes Renal Tubular Regeneration After Renal Ischemia/Reperfusion Injury in Rats

Migita, Heihachi; Yoshitake, Shinji; Tange, Yoshihiro; Choijookhuu, Narantsog; Hishikawa, Yoshitaka

doi:10.5812/numonthly.34421

Cited by 19 publications

(20 citation statements)

References 18 publications

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“…In animal models, HBO has been shown to offer protection from AKI caused by factors such as renal ischemia/reperfusion, rhabdomyolysis‐induced myoglobin and cisplatin‐induced tubular necrosis . It was shown that HBO could induce anti‐oxidant enzyme activity and suppress lipid peroxidation under oxidative stress in AKI .…”

Section: Acute Kidney Injurymentioning

confidence: 99%

“…It was shown that HBO could induce anti‐oxidant enzyme activity and suppress lipid peroxidation under oxidative stress in AKI . Furthermore, HBO was also shown to exert tubular cell regeneration through the inhibition of apoptosis . Although there is scant evidence regarding the effect of HBO on AKI in humans, the application of HBO therapy in the human kidney is expected in the near future.…”

Section: Acute Kidney Injurymentioning

confidence: 99%

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Potential of hyperbaric oxygen in urological diseases

et al. 2019

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Abbreviations & Acronyms AKI = acute kidney injury Alum = aluminium potassium sulfate ATA = atmosphere absolute CR = complete response CRPC = castration-resistant prostate cancer DC = dystrophic calcification EMT = epithelial-tomesenchymal transition FG = Fournier gangrene FGSI = Fournier Gangrene Severity Index HA = hyaluronic acid HBO = hyperbaric oxygen HIC = Hunner type interstitial cystitis IC/PBS = interstitial cystitis/painful bladder syndrome NHIC = non-Hunner type interstitial cystitis PR = partial response RHC = radiation-induced hemorrhagic cystitis ROS = reactive oxygen species RT = radiation therapy TRP = transient receptor potential channel WF10 = immunokine Correspondence: TomoakiAbstract: Hyperbaric oxygen therapy is a promising medical technology that delivers oxygen to targeted tissues at high pressure to increase the amount of dissolved oxygen in the blood. Over the past three decades, hyperbaric oxygen has been used in a variety of conditions, including radiation-induced tissue injuries, non-healing states with ischemia and malignant neoplasms. In the field of urology, hyperbaric oxygen has also been applied to some pathological conditions (e.g. radiation-induced hemorrhagic cystitis, Fournier gangrene, interstitial cystitis, male infertility, acute kidney injury and urological cancers). In normal and injured tissues, hyperoxia from hyperbaric oxygen therapy contributes to anti-inflammation, angiogenesis through endothelial proliferation, enhanced fibroblastic activity, increased lymphocyte and macrophage activity, and bactericidal effects with the aim of wound repair. In cancerous tissues, the enhanced supply of oxygen into the hypoxic cancer cells can exert inhibitory effects on factors that contribute to their aggressiveness (e.g. cell survival, escape from apoptosis, epithelial-to-mesenchymal transition and tumor immunotolerance), and sensitize the tumor to radiation therapy and chemotherapy. However, further research, including multicenter clinical studies, is essential for determining the role of hyperbaric oxygen therapy in refractory urological diseases that are resistant to conventional therapies.

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Section: Acute Kidney Injurymentioning

confidence: 99%

Section: Acute Kidney Injurymentioning

confidence: 99%

Potential of hyperbaric oxygen in urological diseases

et al. 2019

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“…Moreover, the aberrant apoptosis of renal cells, such as tubular cells, due to elevated oxidative stress and enhanced mitochondrial pathway activity has been demonstrated to occur during the pathogenesis of renal iri (8). Several therapeutic reagents and methods that inhibit renal cell apoptosis have demonstrated promising potential as novel treatments for renal iri in animal models, which require further validation; these include hyperbaric oxygen therapy, hydrogen-rich saline and hypothermic machine perfusion (9)(10)(11). investigating the molecular mechanisms that underlie the pharmacological effects of anti-iri drugs may enable the development and clinical application of novel therapies for iri.…”

Section: Introductionmentioning

confidence: 99%

Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation

Kang

Wen

et al. 2020

Mol Med Report

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Penehyclidine hydrochloride (PHc) suppresses renal ischemia and reperfusion (i/r) injury (iri); however, the underlying mechanism of action that achieves this function remains largely unknown. The present study aimed to investigate the potential role of autophagy in PHc-induced suppression of renal iri, as well as the involvement of cell proliferation and apoptosis. a rat iri model and a cellular hypoxia/oxygenation (H/r) model were established; PHc, 3-methyladenine (3-Ma) and rapamycin (rapa) were administered to the iri model rats prior to i/r induction and to H/r cells following reperfusion. Serum creatinine was measured using a biochemistry analyzer, whereas aspartate aminotransferase (aSaT) and alanine aminotransferase (alaT) expression levels were detected using eliSa kits. renal tissue injury was evaluated by histological examination. in addition, microtubule-associated protein light chain 3B (lc3B) expression, autophagosome formation, cell proliferation and apoptosis were detected in the cellular H/r model. The results demonstrated that i/r induced renal injury in iri model rats, upregulated serum creatinine, alaT and aSaT expression levels, and increased autophagic processes. in contrast, pretreatment with PHC or Rapa significantly prevented these i/r-induced changes, whereas the administration of 3-Ma enhanced i/r-induced injuries through suppressing autophagy. PHc and rapa increased lc3B and Beclin-1 expression levels, but decreased sequestome 1 (p62) expression in the cellular H/r model, whereas 3-Ma prevented these PHc-induced changes. PHc and rapa promoted proliferation and autophagy in the cellular H/r model; these effects were accompanied by increased expression levels of lc3B and Beclin-1, and reduced p62 expression levels, whereas these levels were inhibited by 3-Ma. Furthermore, PHc and rapa inhibited apoptosis in the cellular H/r model through increasing Bcl-2 expression levels, and suppressing Bax and caspase-3 expression levels; the opposite effect was induced by 3-Ma. in conclusion, PHc suppressed renal iri through the induction of autophagy, which in turn promoted proliferation and suppressed apoptosis in renal cells.

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“…This therapy enhances the dissolved oxygen concentration in arterial blood and restores the diffusion of oxygen into poorly perfused tissues ( 6 , 7 ). Animal studies have shown that HBO therapy attenuates ischemia reperfusion-induced tissue injury by abating oxidative stress, suppressing inflammation, increasing nitric oxide formation and preventing apoptosis ( 7 - 9 ).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of partial unilateral ureteral obstruction – induced renal damage with hyperbaric oxygen therapy in a rat model

et al. 2017

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Objective:The objective of the present study was to evaluate the effectiveness of HBO therapy on biochemical parameters, renal morphology and renal scintigraphy in rats undergoing chronic unilateral partial ureteral obstruction (UPUO).Material and methods:Thirty-five rats were divided into five equal groups: Control group; Sham group; HBO group; UPUO group and UPUO/HBO group. The effects of HBO therapy were examined using biochemical parameters and histopathological changes. After calculating the score for each histopathological change, the total histopathological score was obtained by adding all the scores. In addition, dynamic renal scintigraphy findings were evaluated.Results:Serum parameters indicating inflammation, serum tumor necrosis factor- alpha, ischemia modified-albumin, IMA/albumin ratio and Pentraxin-3 levels, were observed to be high in the UPUO group and low in the UPUO/HBO treatment group. Similarly, in the treatment group, the reduction in malondialdehyde, total oxidant status and oxidative stress index levels and increase in total antioxidant capacity values were observed to be statistically significant compared to the UPUO group (p<0.001, p=0.007, p<0.001, p=0.001, respectively). The total score and apoptosis index significantly decreased after administration of HBO treatment. Dynamic 99mTc-MAG3 renal scintigraphy also showed convincing evidence regarding the protective nature of HBO against kidney injury. In the UPUO/HBO therapy group, the percentage contribution of each operated kidney increased significantly compared to the UPUO group (41.73% versus 32.72%).Conclusion:The findings of this study indicate that HBO therapy had a reno-protective effect by reducing inflammation and oxidative stress, and preserving renal function after renal tissue damage due to induction of UPUO.

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Hyperbaric Oxygen Therapy Suppresses Apoptosis and Promotes Renal Tubular Regeneration After Renal Ischemia/Reperfusion Injury in Rats

Cited by 19 publications

References 18 publications

Potential of hyperbaric oxygen in urological diseases

Potential of hyperbaric oxygen in urological diseases

Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation

Attenuation of partial unilateral ureteral obstruction – induced renal damage with hyperbaric oxygen therapy in a rat model

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