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

2016 ◽  
Vol 8 (1) ◽  
Author(s):  
Heihachi Migita ◽  
Shigenori Yoshitake ◽  
Yoshihiro Tange ◽  
Narantsog Choijookhuu ◽  
Yoshitaka Hishikawa
Keyword(s):  
Reperfusion Injury ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
Renal Tubular

Hyperbaric Oxygen Therapy Attenuates Renal Ischemia/Reperfusion Injury in Rats

2007 ◽  
Vol 78 (1) ◽  
pp. 82-85 ◽  
Author(s):  
Emrullah Solmazgul ◽  
Gunalp Uzun ◽  
Hakan Cermik ◽  
Enes M. Atasoyu ◽  
Secil Aydinoz ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

scholarly journals Effect of hyperbaric oxygen therapy on the intestinal ischemia reperfusion injury

2011 ◽  
Vol 26 (6) ◽  
pp. 463-469 ◽  
Author(s):  
Rosemary Aparecida Furlan Daniel ◽  
Vinícius Kannen Cardoso ◽  
Emanuel Góis Jr ◽  
Rogério Serafim Parra ◽  
Sérgio Britto Garcia ◽  
...  
Keyword(s):  
Cell Viability ◽  
Reperfusion Injury ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Intestinal Ischemia ◽  
Oxygen Therapy ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Exact Nature ◽  
Intestinal Tissue

PURPOSE: Adequate tissue oxygenation is essential for healing. Hyperbaric oxygen therapy (HBOT) has potential clinical applications to treat ischemic pathologies, however the exact nature of any protective effects are unclear at present. We therefore investigated the potential role of HBOT in modulating the ischemia/reperfusion (I/R) injury response in intestinal model of I/R injury. METHODS: Male Wistar rats were subjected to surgery for the induction of intestinal ischemia followed by reperfusion. HBOT was provided before and/or after intestinal ischemia. Cell viability in the intestinal tissue was assessed using the MTT assay and by measuring serum malondealdehyde (MDA). Microvascular density and apoptosis were evaluated by immunohistochemistry. RESULTS: The results indicate that HBOT treatment pre- and post-ischemia reduces lesion size to the intestinal tissue. This treatment increases cell viability and reduces the activation of caspase-3, which is associated with increased number of tissue CD34 cells and enhanced VEGF expression. CONCLUSION: The hyperbaric oxygen therapy can limit tissue damage due to ischemia/reperfusion injury, by inducing reparative signaling pathways.

scholarly journals HDAC2 targeting stabilizes the CoREST complex in renal tubular cells and protects against renal ischemia/reperfusion injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
David D. Aufhauser ◽  
Paul Hernandez ◽  
Seth J. Concors ◽  
Ciaran O’Brien ◽  
Zhonglin Wang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Tubules ◽  
Renal Protection ◽  
Renal Tubular Cells ◽  
Renal Ischemia Reperfusion Injury ◽  
Renal Tubular

AbstractHistone/protein deacetylases (HDAC) 1 and 2 are typically viewed as structurally and functionally similar enzymes present within various co-regulatory complexes. We tested differential effects of these isoforms in renal ischemia reperfusion injury (IRI) using inducible knockout mice and found no significant change in ischemic tolerance with HDAC1 deletion, but mitigation of ischemic injury with HDAC2 deletion. Restriction of HDAC2 deletion to the kidney via transplantation or PAX8-controlled proximal renal tubule-specific Cre resulted in renal IRI protection. Pharmacologic inhibition of HDAC2 increased histone acetylation in the kidney but did not extend renal protection. Protein analysis demonstrated increased HDAC1-associated CoREST protein in HDAC2-/- versus WT cells, suggesting that in the absence of HDAC2, increased CoREST complex occupancy of HDAC1 can stabilize this complex. In vivo administration of a CoREST inhibitor exacerbated renal injury in WT mice and eliminated the benefit of HDAC2 deletion. Gene expression analysis of endothelin showed decreased endothelin levels in HDAC2 deletion. These data demonstrate that contrasting effects of HDAC1 and 2 on CoREST complex stability within renal tubules can affect outcomes of renal IRI and implicate endothelin as a potential downstream mediator.

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