Zhang Hai-Xia, Du Guan-Hua, Zhang Jun-Tian
National Center for Pharmaceutical Screening, Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences, 1 XiangNongTan Street, Beijing 100050, China.
Neurol Res. 2003 Jul;25(5):471-6. doi: 10.1179/016164103101201878.
It is well known that a brief period of ischemia increases tolerance to a subsequent severe ischemic episode. In the present study, bilateral carotid arteries occlusion (BCAO) was applied as pre-conditioning to testify whether this kind of ischemia could preserve the function of mitochondria with the impairment induced by middle cerebral artery occlusion (MCAO) in brain. The activities of respiratory enzyme complex I to IV, mitochondria swelling, membrane potential, and membrane fluidity were investigated. The results showed that the percentage of infarct area decreased greatly due to the ischemic pre-conditioning (IP) revealing the preventive effect of IP on infarct size. The activities of respiratory enzyme complex III, IV were effectively preserved (p < 0.05, p < 0.05) compared with MCAO group through ischemic pre-conditioning. Mitochondrial swelling and membrane fluidity were protected by IP, and also an increased trend was found in membrane potential, which indicated that the integrity of mitochondrial membrane was maintained. It suggested that the function of mitochondrial energy metabolism in brain ischemia was effectively protected by this kind of pre-conditioning.
众所周知，短暂的缺血期可增强对随后严重缺血发作的耐受性。在本研究中，采用双侧颈动脉闭塞（BCAO）作为预处理，以验证这种缺血是否能在大脑中动脉闭塞（MCAO）诱导的损伤中保护线粒体的功能。研究了呼吸酶复合体I至IV的活性、线粒体肿胀、膜电位和膜流动性。结果表明，由于缺血预处理（IP），梗死面积百分比大幅下降，揭示了IP对梗死大小的预防作用。与MCAO组相比，通过缺血预处理，呼吸酶复合体III、IV的活性得到有效保留（p < 0.05，p < 0.05）。IP保护了线粒体肿胀和膜流动性，膜电位也有增加趋势，这表明线粒体膜的完整性得以维持。这表明这种预处理有效地保护了脑缺血中线粒体能量代谢的功能。
