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Vascul Pharmacol. 2015 Oct;73:86-95. doi: 10.1016/j.vph.2015.04.003. Epub 2015 Apr 22.

Ginsenoside Rb1 attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the JNK and p38 signaling pathways.

Author information

1
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, PR China.
2
Center for Intestinal and Liver Inflammation Research, Stanley Manne Children's Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
3
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, PR China. Electronic address: jbwan@umac.mo.

Abstract

BACKGROUND:

Abdominal aortic aneurysm (AAA), a life-threatening vascular disease, accounts for approximately 10% of the morbidity in people over 65 years old. No satisfactory approach is available to treat AAA. Ginsenosides Rb1 and Rg1 are primary ingredients of Panax notoginseng for the treatment of cardiovascular diseases, but their impact on AAA is unknown.

METHODS AND RESULTS:

An AAA model was established using an Ang II infusion in ApoE(-/-) mice. After continuous stimulation of Ang II for 28 days, suprarenal aortic aneurysms developed in 77% mice and 12% mice died suddenly due to AAA rupture. Administration of ginsenoside Rb1 (20 mg/kg/day), but not ginsenoside Rg1, significantly reduced the incidence and mortality of AAA. Ginsenoside Rb1 treatment dramatically suppressed Ang II-induced diameter enlargement, extracellular matrix degradation, matrix metalloproteinase (MMP) production, inflammatory cell infiltration, and vascular smooth muscle cell (VSMC) dysfunction. Mechanistic studies indicated that the protective effects of ginsenoside Rb1 were associated with the inactivation of JNK and p38 MAPK signaling pathways. A specific activator of JNK and p38, anisomycin, nearly abolished ginsenoside Rb1-driven suppression of MMP secretion by VSMCs.

CONCLUSIONS:

Ginsenoside Rb1, as a potential anti-AAA agent, suppressed AAA through inhibiting the JNK and p38 signaling pathways.

KEYWORDS:

Abdominal aortic aneurysm; Ginsenoside Rb1; Ginsenoside Rb1 (PubChem CID: 9898279); Ginsenoside Rg1 (PubChem CID: 441923); JNK; NF-κB; p38

PMID:
25912763
DOI:
10.1016/j.vph.2015.04.003
[Indexed for MEDLINE]

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