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Hyperbaric Oxygen Therapy Suppresses Apoptosis and Promotes Renal Tubular Regeneration After Renal Ischemia/Reperfusion Injury in Rats
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نویسنده
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Migita Heihachi ,Yoshitake Shigenori ,Tange Yoshihiro ,Choijookhuu Narantsog ,Hishikawa Yoshitaka
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منبع
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nephro-urology monthly - 2016 - دوره : 8 - شماره : 1 - صفحه:1 -5
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چکیده
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Background: renal ischemia/reperfusion (i/r) injury remains a major cause of acute kidney injury (aki), in addition to i/r injury-induced tissue inflammation, necrosis and apoptosis. hyperbaric oxygen therapy (hbo) is defined as a treatment in which a patient is intermittently exposed to 100% oxygen pressurized to a pressure above sea level (> 2.0 atmospheres absolute (ata), 1.0 ata = 760 mmhg). it has been used in a number of medical conditions with a proven efficacy in a limited number of disorders. however, the effects of hbo therapy on apoptosis and proliferative activity after i/r injury have not been fully understood. objectives: we studied the possible beneficial effects of hbo therapy on apoptosis and tubular cell regeneration after renal i/r injury in rats. materials and methods: sprague-dawley (sd) rats were randomized into three groups: sham (sham-operated rats); i/r (animals submitted to i/r); and i/r + hbo (i/r rats exposed to hbo). tubular cell apoptosis was confirmed by dna laddering and the terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end labeling (tunel) assay. cellular proliferation activity was determined using the anti-ki-67 antibody. results: a significant decrease in apoptotic cells and increase in proliferative reaction were observed in the i/r + hbo group compared to the i/r group. conclusions: we demonstrated that hbo suppressed apoptosis, which caused inflammation after renal i/r, and promoted tubular cell regeneration. hbo has protective effects against aki caused by renal i/r through the inhibition of apoptosis.
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کلیدواژه
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Hyperbaric Oxygen Therapy ,Ischemia/Reperfusion Injury ,Apoptosis ,Rats
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آدرس
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Kyushu University of Health and Welfare, Faculty of Health Sciences, Department of Medical Engineering, Japan, Kyushu University of Health and Welfare, Faculty of Health Sciences, Department of Medical Engineering, Japan, Kyushu University of Health and Welfare, Faculty of Health Sciences, Department of Medical Engineering, Japan, University of Miyazaki, Faculty of Medicine, Department of Anatomy, Division of Histochemistry and Cell Biology,, Japan, University of Miyazaki, Faculty of Medicine, Department of Anatomy, Division of Histochemistry and Cell Biology, Japan
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Authors
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