Effect of oxidated low-density lipoprotein on early apoptosis of vascular smooth muscle cell
OBJECTIVE: To investigate the apoptosis in vascular smooth muscle cell (VSMC) induced by oxidated low-density lipoprotein cholesterol (ox-LDL), and to discuss the relative mechanism of the apoptosis of VSMC
Veröffentlicht in: | Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue. - 1998. - 15(2003), 5 vom: 01. Mai, Seite 295-8 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , |
Format: | Aufsatz |
Sprache: | Chinese |
Veröffentlicht: |
2003
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Zugriff auf das übergeordnete Werk: | Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue |
Schlagworte: | English Abstract Journal Article Research Support, Non-U.S. Gov't Lipoproteins, LDL oxidized low density lipoprotein |
Zusammenfassung: | OBJECTIVE: To investigate the apoptosis in vascular smooth muscle cell (VSMC) induced by oxidated low-density lipoprotein cholesterol (ox-LDL), and to discuss the relative mechanism of the apoptosis of VSMC METHODS: The growth index of VSMC of Wistar rat was determined. By using trypan blue to count sustaining cells, the proliferative effect of ox-LDL on culturing VSMC was observed. With flow cytometer, the apoptosis of VSMC induced by ox-LDL and the inhibitory effect of cyclooxygenase-2 (COX-2) inhibitor NS-398 on apoptosis were determined RESULTS: After VSMC grew normally in culture, ox-LDL in concentrations of 35 mg/L and 50 mg/L could advance the growth period of VSMC to between 12 and 24 hours, and the proliferation of VSMC were obvious. The proliferation of VSMC induced by ox-LDL were inhibited by NS-398. The rate of apoptosis of VSMC in ox-LDL and NS-398 groups were higher than that of normal control CONCLUSION: ox-LDL could induce an obvious proliferation of VSMC in culture. Although NS-398 can decrease the proliferation of VSMC, it could enhance ox-LDL to induce apoptosis |
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Beschreibung: | Date Completed 22.10.2012 Date Revised 02.07.2003 published: Print Citation Status MEDLINE |
ISSN: | 1003-0603 |