Koksel Oguz, Kaplan Murat Bayram, Ozdulger Ali, Tamer Lulufer, Degirmenci Ulas, Cinel Leyla, Bastürk Mine, Kanik Arzu
Department of Thoracic Surgery, Mersin University, School of Medicine, 33079 Mersin, Turkey.
Exp Lung Res. 2005 Jun;31(5):483-96. doi: 10.1080/01902140590918876.
Caffeic acid phenethyl ester (CAPE) is a phenolic antioxidant and is an active anti-inflammatory component of honeybee propolis. The authors evaluated the effects of CAPE on oxidative stress and lung damage in an oleic acid (OA)-induced lung-injury model. Rats were divided into 5 groups as sham, OA, CAPE, pre-OA-CAPE, and post-OA-CAPE. Acute lung injury was induced by intravenous administration of 100 mg/kg of OA. Pre-OA-CAPE group received CAPE (10 micromol/kg. intravenously) 15 minutes before OA infusion and post-OA-CAPE group received CAPE 2 hours after OA administration. Malondialdehyde (MDA) level of plasma, bronchoalveolar lavage fluid (BALF), and lung tissue; myeloperoxidase activity of BALF and lung tissue; Na(+)-K(+) ATPase activity of lung tissue; and total protein content of BALF were measured. Light microscopic analyses of lung specimens were performed. The increased MDA levels in lung homogenates (47.98+/-13.75 nmol/mL), BALF (31.12+/-3.07 nmol/mL), and plasma (61.84+/-15.34 nmol/mL) decreased significantly to 24.33+/-3.09 nmol/mL (P = 0.000), 23.19+/-4.97 nmol/mL (P = 0.002), and 27.36+/-5.37 nmol/mL (P = 0.000), respectively, following CAPE administration in pre-OA-CAPE group. Another important finding was the restoration of the enzymatic activity of Na(+)-K(+) ATPase from a value of 203.89+/-32.18 nmol Pi/mg Protein/h in OA group, to a value of 302.17+/-51.90 nmol Pi/mg Protein/h (P = 0.012) in pre-OA-CAPE group with CAPE treatment. CAPE has been shown to have a clear attenuating effect on oxidative damage in experimental animal studies. However, further investigations are necessary to suggest CAPE as a treatment agent in critically ill patients with lung injury.
咖啡酸苯乙酯（CAPE）是一种酚类抗氧化剂，是蜜蜂蜂胶中的一种活性抗炎成分。作者在油酸（OA）诱导的肺损伤模型中评估了CAPE对氧化应激和肺损伤的影响。将大鼠分为5组：假手术组、OA组、CAPE组、OA前CAPE组和OA后CAPE组。通过静脉注射100 mg/kg的OA诱导急性肺损伤。OA前CAPE组在注入OA前15分钟静脉注射CAPE（10 μmol/kg），OA后CAPE组在OA给药后2小时接受CAPE。检测血浆、支气管肺泡灌洗液（BALF）和肺组织中的丙二醛（MDA）水平；BALF和肺组织中的髓过氧化物酶活性；肺组织中的Na(+)-K(+) ATP酶活性；以及BALF中的总蛋白含量。对肺标本进行光镜分析。OA组肺匀浆（47.98±13.75 nmol/mL）、BALF（31.12±3.07 nmol/mL）和血浆（61.84±15.34 nmol/mL）中升高的MDA水平在OA前CAPE组给予CAPE后分别显著降低至24.33±3.09 nmol/mL（P = 0.000）、23.19±4.97 nmol/mL（P = 0.002）和27.36±5.37 nmol/mL（P = 0.000）。另一个重要发现是，OA前CAPE组经CAPE治疗后，Na(+)-K(+) ATP酶的酶活性从OA组的203.89±32.18 nmol Pi/mg蛋白/h恢复到302.17±51.90 nmol Pi/mg蛋白/h（P = 0.012）。在实验动物研究中，CAPE已显示出对氧化损伤有明显的减轻作用。然而，有必要进行进一步研究，以推荐将CAPE作为肺损伤重症患者的治疗药物。
