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目的:初步研究阿霉素导致血管壁脂质过氧化状态下纤连蛋白(fibronectin,FN)及P105基因表达的变化及其意义,并对动脉粥样硬化患者的临床康复介入提供理论依据。方法:将雄性SD大鼠40只随机分成4组,每组10只:正常对照组,阿霉素低剂量组(10mg/kg),阿霉素中剂量组(20mg/kg),阿霉素高剂量组(40mg/kg),对后3组分别一次性腹腔注射不同剂量的阿霉素,制备脂质过氧化模型。采用硫代巴比妥酸(Thiobarbituricacid,TBA)荧光分光光度法测定大鼠血清脂质过氧化产物丙二醛含量。运用反转录聚合酶链反应(RT-PCR)测定大鼠主动脉中的纤连蛋白(Fibronectin,FN)、P105共活化因子mRNA的表达。结果:对照组、阿霉素低、中、高剂量组大鼠血清丙二醛的含量分别为(12.6±3.8),(17.4±2.9),(20.9±3.4),(24.5±4.1)μmol/L,其中中、高剂量组大鼠血清中丙二醛含量高于对照组(t=2.27,P<0.05;t=2.89,P<0.01);RT-PCR结果表明FN,P105mRNA在不同剂量模型组呈不同程度的高表达。结论:在阿霉素导致血管壁损伤后,有FN,P105基因的高表达,脂质过氧可能通过多种途径诱导动脉粥样硬化的形成。
OBJECTIVE: To study the changes of fibronectin (FN) and P105 gene expression induced by doxorubicin in vascular lipid peroxidation and to provide a theoretical basis for the clinical rehabilitation of patients with atherosclerosis. Methods: Forty male SD rats were randomly divided into 4 groups with 10 rats in each group: normal control group, low dose doxorubicin group (10mg / kg), middle dose of doxorubicin group (20mg / kg) High dose group (40mg / kg), the latter three groups were intraperitoneal injection of different doses of doxorubicin, lipid peroxidation model. Thiobarbituric acid (Thiobarbituric acid, TBA) fluorescence spectrophotometry was used to determine the level of malondialdehyde (MDA) in rat serum. The expression of Fibronectin (FN) and P105 coactivator mRNA in the aorta of rats was determined by reverse transcription-polymerase chain reaction (RT-PCR). Results: The contents of malondialdehyde in the control group, adriamycin low, middle and high dose groups were (12.6 ± 3.8), (17.4 ± 2.9), (20.9 ± 3.4) and (24.5 ± 4.1) μmol / L, the content of malondialdehyde in middle and high dose group was higher than that in control group (t = 2.27, P <0.05; t = 2.89, P <0.01) Group showed varying degrees of high expression. Conclusion: After doxorubicin causes vascular wall injury, there is high expression of FN and P105 genes. Lipid peroxidation may induce the formation of atherosclerosis in many ways.