摘要
研究脑缺血再灌流时线粒体磷脂含量与膜流动性改变,结果发现缺血20min再灌流1h组线粒体卵磷脂(PC)、脑磷脂(PE)、心磷脂(CL)含量与膜流动性均显著降低,磷脂酶C(PLC)抑制剂苯甲基碘酰氟化物(PMSF)治疗组线粒体PC、PE、CL含量与膜流动性均明显增高,并能显著地减轻海马CA1区迟发性神经元坏死,提示线粒体磷脂含量与膜的流动性密切相关,肌醇磷脂信使系统参与了缺血性脑损伤。
In order to elucidate the role of phosphoinositide transduction system played in the mitochondrial damages during cerbral ischemia-reperfusion injury,the changes of phospholipids and membrane fluidity of the mitochondria were observed.It was found that the phospholipid level and mitochondrial membrane fluidity were decreased significantly in the lst h after reperfusion and came up later to the level of SAM group.In addition,treatment with PMSF could increase phospholipid level, improve mitochondrial mebrane fluidity and attenuate the severity of delayed death of CA1 pyramidal cells in the hippocampus.These findings suggest that the damages to the mitochondria during cerebral ischemia-reperfusion injury are closely related to the level of mitochondrial phospholipids.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1996年第1期13-15,共3页
Journal of Third Military Medical University
基金
国家自然科学基金
关键词
脑缺血
再灌流
线粒体
磷脂
膜流动性
cerebral ischemia and reperfusion
mitochondrion
phospholipid
membrane fluidity
PMSF