用DPPH自由基损伤血管内皮细胞功能的新方法

A NEW METHOD INDUCING DYSFUNCTION OF ENDOTHELIUM-DEPENDENT RELAXATION BY DPPH FREE RADICAS

本研究在兔胸主动脉环模型上观察了二苯三硝基苯肼（ＤＰＰＨ）自由基对乙酰胆碱（ＡＣｈ）诱导的血管内在依赖性舒张（ＥＤＲ）反应的影响。结果显示：０．２５μｍｏｌ·Ｌ－１ＤＰＰＨ与血管环孵育１０ｍｉｎ，显著抑制了ＡＣｈ诱导的血管ＥＤＲ反应。此种抑制作用为可逆性。拉米普利和缓激肽能显著保护ＤＰＰＨ损伤的血管ＥＤＲ反应。用ＤＰＰＨ建立自由基损伤模型的方法具有简单、方便、可靠、重复性好等优点。

he present paper describes for the first time a new simplemethod for damaging the en-dothelium cell(EC)-dependent relaxation by free radicals in vitro.The acetylcholine(ACh)-in-duced EC-dependent relaxation of rabbit aortic rings were injured in tissure bath by exposing for10 min to 0. 25μmol·L-1,1-Dipheny l-2-Picryl-Hydrazyl (DPPH), a stable free radicas. TheACh-induced relaxation was reduced from 89.3±1.6%to 36.1±3.2%immediately after l0minexposure to DPPH,and it gradually recovered to 43.3±2.1%and 54. 4±2.2%30 min and 60min respectively after washing out of DPPH, So the damage is reversible. The effecacy of thismodel was confirmed by the protective effect against the DPPH free radical damage provided by 5μmol·L -1 ramiprilat, an active form of ACE inhibitor ramipral or 1 μmol·L-1 bradykinine.This new method is simple, reliable and reproducible.