Effect of lipanthyl on mRNA expression of endothelin-1 and nitric-oxide synthase in atherosclerotic vessel wall in rabbits.

Abstract

AIM:

To study the mechanism of regression of atherosclerosis (AS) by lipanthyl.

METHODS:

Experimental atherosclerotic rabbits created by damaging the abdominal aortic endothelium and feeding with high fat diet for 8 wk were then treated with lipanthyl 15 mg.kg-1.d-1 for 16 wk. Expression of endothelin (ET)-1 mRNA and nitric oxide synthase (NOS) mRNA in atherosclerotic vessel wall was measured by in situ hybridization and reverse transcription polymerase chain reaction (RT-PCR), respectively.

RESULTS:

After lipanthyl administration for 16 wk, ET-1 mRNA expression was reduced, and integral optical density (IOD) and area of hybridization granule were observed to be (49,113 +/- 16,868) and (2448 +/- 621) micron 2 in lipanthyl group and (65,188 +/- 10,113) and (3028 +/- 352) micron 2 in atherosclerotic group, respectively. Regarding inducible NOS mRNA expression, IOD and area were decreased by 25.5% and 53.3%, respectively, whereas endothelial NOS mRNA expression was increased.

CONCLUSION:

Restoration of the disturbed ET-1 mRNA/NOS mRNA balance by lipanthyl might be one of its mechanisms leading to regression of atherosclerosis.

• Authors: M L Xie, Z L Gu, K J Chen, W X Zhou, C Y Guo
• Journal: Acta pharmacologica Sinica (Acta Pharmacol Sin) Vol. 21 Issue 5 Pg. 473-6 (May 2000) ISSN: 1671-4083 [Print] United States
• PMID: 11324450 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Endothelin-1
• Hypolipidemic Agents
• RNA, Messenger
• Nitric Oxide Synthase
• Nitric Oxide Synthase Type II
• Fenofibrate

Topics

• Animals
• Aorta, Abdominal (metabolism)
• Arteriosclerosis (metabolism)
• Endothelin-1 (biosynthesis, genetics)
• Fenofibrate (pharmacology)
• Hypolipidemic Agents (pharmacology)
• Male
• Nitric Oxide Synthase (biosynthesis, genetics)
• Nitric Oxide Synthase Type II
• RNA, Messenger (biosynthesis, genetics)
• Rabbits
• Random Allocation