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Arctium lappa ameliorates endothelial dysfunction in rats fed with high fat/cholesterol diets

BACKGROUND: Arctium lappa L. (Asteraceae), burdock, is a medicinal plant that is popularly used for treating hypertension, gout, hepatitis, and other inflammatory disorders. This study was performed to test the effect of ethanol extract of Arctium lappa L. (EAL) seeds on vascular reactivity and infl...

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Detalles Bibliográficos
Autores principales: Lee, Yun Jung, Choi, Deok Ho, Cho, Guk Hyun, Kim, Jin Sook, Kang, Dae Gill, Lee, Ho Sub
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517347/
https://www.ncbi.nlm.nih.gov/pubmed/22866890
http://dx.doi.org/10.1186/1472-6882-12-116
Descripción
Sumario:BACKGROUND: Arctium lappa L. (Asteraceae), burdock, is a medicinal plant that is popularly used for treating hypertension, gout, hepatitis, and other inflammatory disorders. This study was performed to test the effect of ethanol extract of Arctium lappa L. (EAL) seeds on vascular reactivity and inflammatory factors in rats fed a high fat/cholesterol diet (HFCD). METHOD: EAL-I (100 mg·kg(−1)/day), EAL-II (200 mg·kg(−1)/day), and fluvastatin (3 mg·kg(−1)/day) groups initially received HFCD alone for 8 weeks, with EAL supplementation provided during the final 6 weeks. RESULTS: Treatment with low or high doses of EAL markedly attenuated plasma levels of triglycerides and augmented plasma levels of high-density lipoprotein (HDL) in HFCD-fed rats. Chronic treatment with EAL markedly reduced impairments of acetylcholine (ACh)-induced relaxation of aortic rings. Furthermore, chronic treatment with EAL significantly lowered systolic blood pressure (SBP) and maintained smooth and flexible intimal endothelial layers in HFCD-fed rats. Chronic treatment with EAL suppressed upregulation of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and E-selectin in the aorta. Chronic treatment with EAL also suppressed increases in matrix metalloproteinase (MMP)-2 expression. These results suggested that EAL can inhibit HFCD-induced vascular inflammation in the rat model. CONCLUSION: The present study provides evidence that EAL ameliorates HFCD-induced vascular dysfunction through protection of vascular relaxation and suppression of vascular inflammation.