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[动脉粥样硬化中p53抑癌基因的突变与血清脂质水平之间的关系]

[The relations between mutations of p53 anti-oncogene in atherosclerosis and levels of lipids in serum].

作者信息

Wang Y, Li T, Deng X

机构信息

Department of Cardiology, PLA General Hospital, Beijing.

出版信息

Zhonghua Yi Xue Za Zhi. 1997 Jul;77(7):501-4.

PMID:9772449
Abstract

OBJECTIVE

To further understanding the pathogenesis of human atherosclerosis, we studied the mutations of p53 anti-oncogene in Chinese atherosclerosis lesions and the relations between p53 gene mutations with the levels of serum lipoprotein and the contents of lipids in AS tissues.

METHODS

p53 gene mutations were detected by a-32P-dCTP labelled radiative PCR-SSCP and the biochemical analyses of lipids in serum and AS tissues.

RESULTS

In 89 cases studied, 9 were found the p53 gene multi-hotsports exons mutations. The TC, TG and CE contents in vascular AS tissues in p53 gene mutation group were higher than those in non-mutations group (ANOV: F = 4.56-9.97, P < 0.05-0.01, no differences in PL contents). But there were no statistic differences in serum levels of TC, TG, CE and apoAI between the two groups (P > 0.05-0.25). All the levels of the serum lipoproteins studied were almost in normal ranges.

CONCLUSION

The DNA structural mutations of p53 anti-oncogene in Chinese adults' AS tissues have remarkable relations with the severity of AS lesions. The mutations of p53 gene may play some important roles in the formation of human atherosclerosis. In addition to serum lipid disorders, this may be a new mechanism in the pathogenesis of human atherosclerosis.

摘要

目的

为进一步了解人类动脉粥样硬化的发病机制,我们研究了中国动脉粥样硬化病变中p53抑癌基因的突变情况,以及p53基因突变与血清脂蛋白水平和动脉粥样硬化(AS)组织中脂质含量之间的关系。

方法

采用α-32P-dCTP标记的放射性聚合酶链反应-单链构象多态性(PCR-SSCP)检测p53基因突变,并对血清和AS组织中的脂质进行生化分析。

结果

在研究的89例病例中,发现9例存在p53基因多热点外显子突变。p53基因突变组血管AS组织中的总胆固醇(TC)、甘油三酯(TG)和胆固醇酯(CE)含量高于非突变组(方差分析:F = 4.56 - 9.97,P < 0.05 - 0.01,磷脂(PL)含量无差异)。但两组间血清TC、TG、CE和载脂蛋白AI(apoAI)水平无统计学差异(P > 0.05 - 0.25)。所研究的血清脂蛋白水平均几乎在正常范围内。

结论

中国成年人AS组织中p53抑癌基因的DNA结构突变与AS病变的严重程度有显著关系。p53基因的突变可能在人类动脉粥样硬化的形成中起重要作用。除了血清脂质紊乱外,这可能是人类动脉粥样硬化发病机制中的一种新机制。

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