Cebi Gamze, Yildiz Şenol, Uzun Gunalp, Oztas Yeşim, Sabuncuoglu Suna, Kutlu Ayhan, Ilgaz Yasin, Karatop-Cesur Iclal, Dogan Eyup, Oztas Emin
a Department of Undersea and Hyperbaric Medicine , Gülhane Military Medical Academy , Ankara , Turkey.
b Department of Biochemistry, Faculty of Medicine , Hacettepe University , Ankara , Turkey.
Ren Fail. 2016 Oct;38(9):1554-1559. doi: 10.1080/0886022X.2016.1227925. Epub 2016 Oct 20.
Myoglobinuric acute renal failure (MARF) may develop after severe muscle injury. Heme oxygenase-1 (HO-1), a stress-response protein, has been implicated as a protective agent against MARF. We hypothesized that hyperbaric oxygen therapy (HBOT) may alleviate MARF by inducing renal HO-1 expression. Wistar-Albino rats were randomly assigned into three groups: Control (n = 4), MARF (n = 8), MARF + HBO (n = 8). MARF was induced by intramuscular glycerol (50%, 8 mL/kg) injection. Saline (8 mL/kg) was injected into the hind limb of the animals in the control group. Animals in the MARF + HBO group received two sessions of HBO therapy (90 min at 2.5 atm) 2 and 18 h after glycerol injection. Serum and tissue samples were taken at 24 h. Serum urea and creatinine levels increased in the MARF and MARF + HBO groups confirming the development of MARF. But, serum urea and creatinine levels were similar in MARF and MARF + HBO groups. Oxidative stress parameters were similar among all groups. Histological renal injury score was similar in MARF and MARF + HBO groups. HO-1 level, determined by immunohistochemistry, was significantly higher in MARF and MARF + HBO groups, compared to the control group. Although HO-1 level in MARF + HBO group was higher than MARF group, it was not statistically significant. We found that HBOT did not reduce renal injury in experimental MARF model. HBOT is used to reduce the muscle damage after crush injury, which may be accompanied by MARF. Therefore, more studies are needed to understand the effects of HBO treatment on renal functions after MARF.
肌红蛋白尿性急性肾衰竭（MARF）可能在严重肌肉损伤后发生。血红素加氧酶-1（HO-1）是一种应激反应蛋白，被认为是对抗MARF的保护因子。我们推测高压氧治疗（HBOT）可能通过诱导肾脏HO-1表达来减轻MARF。将Wistar-白化大鼠随机分为三组：对照组（n = 4）、MARF组（n = 8）、MARF + HBO组（n = 8）。通过肌肉注射甘油（50%，8 mL/kg）诱导MARF。向对照组动物的后肢注射生理盐水（8 mL/kg）。MARF + HBO组动物在甘油注射后2小时和18小时接受两疗程的HBOT治疗（2.5个大气压下90分钟）。在24小时采集血清和组织样本。MARF组和MARF + HBO组的血清尿素和肌酐水平升高，证实了MARF的发生。但是，MARF组和MARF + HBO组的血清尿素和肌酐水平相似。所有组的氧化应激参数相似。MARF组和MARF + HBO组的组织学肾损伤评分相似。通过免疫组织化学测定的HO-1水平，与对照组相比，MARF组和MARF + HBO组显著更高。虽然MARF + HBO组的HO-1水平高于MARF组，但差异无统计学意义。我们发现HBOT在实验性MARF模型中并未减轻肾损伤。HBOT用于减轻挤压伤后可能伴有MARF的肌肉损伤。因此，需要更多研究来了解HBOT治疗对MARF后肾功能的影响。
