Effect of Methanol Extract of Sorbus Cortex in a Rat Model of L-NAME-Induced Atherosclerosis

• Published in: Biological & Pharmaceutical Bulletin 2005, Vol.28(7), pp.1239-1243
• Main Authors: Sohn, Eun Jin, Kang, Dae Gill, Choi, Deok Ho, Lee, An Sook, Mun, Yeon Ja, Woo, Won Hong, Kim, Jin Sook, Lee, Ho Sub
• Format: Article
• Language: English
• Subjects: Animals; Arteriosclerosis - chemically induced; Arteriosclerosis - enzymology; Arteriosclerosis - metabolism; atherosclerosis; Base Sequence; Cell Adhesion Molecules - metabolism; Chemokine CCL2 - metabolism; DNA Primers; Endothelin-1 - genetics; Methanol - chemistry; NF-kappa B - metabolism; NG-nitro-L-arginine methyl ester (L-NAME); NG-Nitroarginine Methyl Ester - toxicity; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type III; Plant Extracts - pharmacology; Rats; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Sorbus - chemistry; Sorbus commixta cortex; Transcription Factor RelA
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.28.1239

Chronic inhibition of nitric oxide (NO) synthesis by administration of high dose of NG-nitro-L-arginine methylester (L-NAME) induces vascular inflammation and subsequent atherosclerosis. We aimed to investigate whether the methanol extract of Sorbus commixta cortex (MSC) is able to prevent inflammatory process in a rat model of L-NAME-induced atherosclerosis. Chronic treatment with low or high doses of MSC prevented the L-NAME-induced increase in monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-κB (NF-κB) p65 expressions as well as adhesion molecules including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in aorta. In addition, increased endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) expressions and decreased endothelial cell NO synthase (ecNOS) expression in aorta from L-NAME treated group was reversed by treatment with MSC. From the histological examination, aortic segment from the L-NAME-treated rats revealed a thickening of intima and media, which was ameliorated by treatment with MSC. In conclusion, our results indicate that MSC can prevent atherosclerosis by inhibiting vascular over-expressions of vasoactive materials, pro-inflammatory transcription factor, and adhesion molecules and by augmenting ecNOS in chronic L-NAME-treated rat model.