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高压氧疗法可抑制大鼠肾缺血/再灌注损伤后的细胞凋亡并促进肾小管再生。

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

作者信息

Migita Heihachi, Yoshitake Shigenori, Tange Yoshihiro, Choijookhuu Narantsog, Hishikawa Yoshitaka

机构信息

Department of Medical Engineering, Faculty of Health Sciences, Kyushu University of Health and Welfare, Yoshinomachi, Nobeoka, Japan.

Department of Anatomy, Faculty of Medicine, Division of Histochemistry and Cell Biology, University of Miyazaki, Kyotake, Miyazaki, Japan.

出版信息

Nephrourol Mon. 2016 Jan 17;8(1):e34421. doi: 10.5812/numonthly.34421. eCollection 2016 Jan.

Abstract

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.

摘要

背景

除了缺血/再灌注(I/R)损伤诱导的组织炎症、坏死和凋亡外,肾缺血/再灌注损伤仍是急性肾损伤(AKI)的主要原因。高压氧治疗(HBO)被定义为一种治疗方法,即患者间歇性暴露于加压至高于海平面压力的100%氧气中(>2.0绝对大气压(ATA),1.0 ATA = 760 mmHg)。它已被用于多种医疗状况,在少数疾病中已证实具有疗效。然而,HBO治疗对I/R损伤后细胞凋亡和增殖活性的影响尚未完全了解。

目的

我们研究了HBO治疗对大鼠肾I/R损伤后细胞凋亡和肾小管细胞再生的可能有益作用。

材料和方法

将Sprague-Dawley(SD)大鼠随机分为三组:假手术组(假手术大鼠);I/R组(接受I/R的动物);I/R + HBO组(接受HBO治疗的I/R大鼠)。通过DNA梯状条带分析和末端脱氧核苷酸转移酶介导的三磷酸尿苷缺口末端标记(TUNEL)测定法确认肾小管细胞凋亡。使用抗Ki-67抗体测定细胞增殖活性。

结果

与I/R组相比,I/R + HBO组凋亡细胞显著减少,增殖反应增加。

结论

我们证明HBO抑制了肾I/R后引起炎症的细胞凋亡,并促进了肾小管细胞再生。HBO通过抑制细胞凋亡对肾I/R引起的AKI具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a8f/4780282/1b39a6dddaa5/num-08-01-34421-g001.jpg

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