Yonehana T, Gemba M
Division of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan.
Jpn J Pharmacol. 1995 Jun;68(2):231-4. doi: 10.1254/jjp.68.231.
The aim of this study was to characterize injuries of LLC-PK1 and MDCK cells exposed to hypoxia and reoxygenation. Exposure of LLC-PK1 cells to hypoxia reduced the ATP contents and increased the leakage of lactate dehydrogenase (LDH), but MDCK cells had no such injuries. Hypoxia-reoxygenation of LLC-PK1 cells dramatically increased LDH leakage, which was suppressed by free radical scavengers, N,N'-diphenyl-p-phenylenediamine, superoxide dismutase and N,N'-dimethylthiourea. These results suggest that use of LLC-PK1 cells has advantages for the investigation of ischemia-reperfusion injury of the kidney as an in vitro model and that generation of oxygen radicals is involved in the cellular injury induced by hypoxia-reoxygenation.
本研究的目的是描述暴露于缺氧和复氧环境下的LLC-PK1和MDCK细胞的损伤情况。将LLC-PK1细胞暴露于缺氧环境会降低ATP含量并增加乳酸脱氢酶(LDH)的泄漏,但MDCK细胞没有此类损伤。LLC-PK1细胞的缺氧复氧显著增加了LDH泄漏,自由基清除剂N,N'-二苯基对苯二胺、超氧化物歧化酶和N,N'-二甲基硫脲可抑制这种泄漏。这些结果表明,使用LLC-PK1细胞作为体外模型来研究肾脏缺血再灌注损伤具有优势,并且氧自由基的产生参与了缺氧复氧诱导的细胞损伤。