Jeon D S, Ha E Y, Mun K C
Institute for Medical Science, Keimyung University, Daegu, Korea.
Transplant Proc. 2012 May;44(4):988-90. doi: 10.1016/j.transproceed.2012.01.091.
Some of the airway complications relate to the use of cyclosporine (CsA), a potent agent widely used after organ transplantations. Several recent studies have demonstrated CsA treatment to induce reactive oxygen species (ROS). The present study was undertaken to investigate effects of CsA on production of ROS and antoxidant defense of airway cells using the human bronchial epithelial cell line BEAS-2B.
We measured biological antioxidant potential (BAP), as well as ROS and malondialdehyde levels in BEAS-2B cells after CsA treatment, using Free Radical Analytical System 4 kits (Diacron, Grosseto, Italy). ROS production was expressed as Carr Units as established by the manufacturer and BAP as μmol/2 × 10(5) cells; malondialdehyde, by the thiobarbituric acid assay.
ROS production was increased in the BEAS-2B cells after CsA treatment: 73.5 at 0 (controls); 82.5 at 10; 84.0 at 30; 86.0 at 50; and 93.0 Carr Unit/2 × 10(5) cells at 100 μg/mL of CsA. The levels of BAP were 1821 at 0 (controls), 1698 at 10; 1653 at 30; 1366 at 50 μg/mL; and 1391 at 100 μg/mL. The levels of malondialdehyde were increased: 3.8 at 0 (controls); 3.4 at 10; 4.4 at 30; 4.2 at 50: and 5.0 nmol/10(6) cells at 100 μg/mL.
Increased production of ROS and decreased BAP by CsA in BEAS-2B cells may increase malondialdehyde levels by radical-induced damage.
一些气道并发症与环孢素(CsA)的使用有关,CsA是器官移植后广泛使用的一种强效药物。最近的几项研究表明,CsA治疗可诱导活性氧(ROS)产生。本研究旨在利用人支气管上皮细胞系BEAS-2B,研究CsA对气道细胞ROS产生和抗氧化防御的影响。
我们使用自由基分析系统4试剂盒(意大利格罗塞托的迪亚克龙公司),测量了CsA处理后BEAS-2B细胞中的生物抗氧化能力(BAP)以及ROS和丙二醛水平。ROS产生量以制造商规定的卡尔单位表示,BAP以μmol/2×10⁵细胞表示;丙二醛通过硫代巴比妥酸测定法测定。
CsA处理后,BEAS-2B细胞中的ROS产生量增加:0(对照)时为73.5;10μg/mL时为82.5;30μg/mL时为84.0;50μg/mL时为86.0;100μg/mL的CsA时为93.0卡尔单位/2×10⁵细胞。BAP水平在0(对照)时为1821,10μg/mL时为1698;30μg/mL时为1653;50μg/mL时为1366;100μg/mL时为1391。丙二醛水平升高:0(对照)时为3.8;10μg/mL时为3.4;30μg/mL时为4.4;50μg/mL时为4.2;100μg/mL时为5.0nmol/10⁶细胞。
CsA使BEAS-2B细胞中ROS产生增加和BAP降低,可能通过自由基诱导的损伤增加丙二醛水平。