摘要
目的探讨载脂蛋白J(ApoJ)在大鼠脑梗死急性期的作用及其机制。方法清洁级SD雄性成年大鼠70只,随机分为正常对照组、假手术组、脑梗死后6 h组、24 h组、3 d组、5 d组和7 d组。用线栓法制备永久性局灶性脑梗死模型,动物处死后检测ApoJ及补体C3mRNA的表达值。结果各模型组手术侧ApoJ mRNA表达和C3mRNA表达水平均高于正常对照组及假手术组(P<0.01),C3的表达从脑缺血后6 h起高于对照组,而ApoJ在缺血后24 h才出现表达增强。ApoJ mRNA表达值与补体C3 mRNA表达水平呈正相关(r=0.427,P<0.01)。结论大鼠脑梗死后补体C3激活,ApoJ的表达代偿性增高,以抑制补体的活性,从而抑制补体介导的神经元死亡,起神经元保护的作用。
Objective To investigate the mechanism of the neuroprotective effect of ApoJ in rat acute cerbral infarction. Methods 70 healthy male SD rats were divided randomly into normal control group, shamoperated group, cerebral infarction 6 hour group, 24 hour group, 3 day group, 5 day group and 7 day group. Permanent cerebral infarction models were prepared by occluding the middle cerebral artery (MCA) using thread embolizing, the C3 and ApoJ mRNA expression was analyzed by RT-PCR. Results An in-creased expression was found in isehemia rat brain and a low level expression ApoJ mRNA was detected in normal rat brain, a positive correlation found between C3 mRNA and ApoJ mRNA expression ( r = 0.427, P 〈 0. 01 ). Conclusions Increased ApoJ expression may be invoved in neuroproteetion in cerebral infarction by inhibiting the complement activation.
出处
《辽宁医学院学报》
CAS
2008年第4期308-310,384,共4页
Journal of Liaoning Medical University (LNMU) Bimonthly
关键词
载脂蛋白J
补体C3
脑梗死
ApoJ
complement component C3
cerebral infarction