Tsai Shen-Kou, Lin Min-Jon, Liao Pei-Hu, Yang Chi-Yea, Lin Su-Man, Liu Sheng-Ming, Lin Ruey-Hseng, Chih Chun-Lien, Huang Shiang-Suo
Department of Anesthesiology, College of Medicine, Buddhist Tzu-Chi University and Hospital, National Taiwan University, Taipei Veterans General Hospital, Taipei, Taiwan.
Life Sci. 2006 May 1;78(23):2758-62. doi: 10.1016/j.lfs.2005.10.017. Epub 2005 Nov 21.
The effects of caffeic acid phenethyl ester (CAPE), an antioxidant derived from propolis, on the infarct volume elicited by focal cerebral ischemia were studied on Long-Evans rats. Cerebral infarction was induced by microsurgical procedures with ligation of the right middle cerebral artery (MCA) and clipping of bilateral common carotid arteries (CCA) for 60 min. The rats were sacrificed 24 h later and serial brain slices of 2 mm thickness were taken and stained for the measurement of infarct area. CAPE was administered intravenously 15 min before MCA occlusion. Pretreatment of CAPE (0.1, 1 and 10 microg/kg) significantly reduced the total infarct volume from 169.6 +/- 14.5 mm3 (control) to 61.0 +/- 24.1 mm3 (0.1 microg/kg CAPE), 47.4 +/- 9.1 mm3 (1 microg/kg CAPE), and 42.4 +/- 8.7 mm3 (10 microg/kg CAPE), respectively. Plasma nitric oxide (NO) content was significantly increased in rats subjected to focal cerebral ischemia. It is concluded that CAPE possesses neuroprotective properties in focal cerebral ischemia injury in rats possibly through its antioxidant effect and/or via the upregulation of NO production.
在Long-Evans大鼠身上研究了蜂胶来源的抗氧化剂咖啡酸苯乙酯(CAPE)对局灶性脑缺血引起的梗死体积的影响。通过显微手术结扎右侧大脑中动脉(MCA)并夹闭双侧颈总动脉(CCA)60分钟诱导脑梗死。24小时后处死大鼠,取2毫米厚的连续脑切片并染色以测量梗死面积。在MCA闭塞前15分钟静脉注射CAPE。CAPE(0.1、1和10微克/千克)预处理显著降低了总梗死体积,分别从169.6±14.5立方毫米(对照组)降至61.0±24.1立方毫米(0.1微克/千克CAPE)、47.4±9.1立方毫米(1微克/千克CAPE)和42.4±8.7立方毫米(10微克/千克CAPE)。局灶性脑缺血大鼠的血浆一氧化氮(NO)含量显著增加。得出的结论是,CAPE在大鼠局灶性脑缺血损伤中具有神经保护特性,可能是通过其抗氧化作用和/或通过上调NO生成来实现。