Inhibition of angiotensin-converting enzyme protects endothelial cell against hypoxia/reoxygenation injury
作者:Noriko Fujita、Hiroki Manabe、Norimasa Yoshida、Naohito Matsumoto、Jun Ochiai、Yasuharu Masui、Manabu Uemura、Yuji Naito、Toshikazu Yoshikawa
DOI:10.1002/biof.5520110404
日期:——
suicide pathway leading to apoptosis of HAEC by enhancing caspase-3 activity, while subsequent reoxygenation induced necrosis by enhancing oxygen radical production. Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide.
血管紧张素转换酶(ACE)抑制剂可预防缺血/再灌注中的心血管组织损伤。但是,尚未详细评估内皮细胞的机制。培养的人主动脉内皮细胞(HAEC)在有或没有复氧的情况下暴露于缺氧状态。缺氧增强了细胞凋亡以及caspase-3的激活。复氧增加了乳酸脱氢酶的释放时间,并伴随着细胞内氧自由基的增加。ACE抑制剂奎那普利拉和缓激肽可显着减少细胞凋亡和乳酸脱氢酶的释放,而激肽B2受体拮抗剂和一氧化氮合酶抑制剂可降低这些作用。总之,缺氧通过增强caspase-3活性激活了自杀途径,导致HAEC凋亡,而随后的复氧通过增强氧自由基的产生而引起坏死。奎那普利拉可以通过增加缓激肽而上调组成型内皮型一氧化氮合酶,从而改善细胞凋亡和坏死,从而增加一氧化氮。