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Int J Cardiol. 2013 Oct 3;168(3):2498-505. doi: 10.1016/j.ijcard.2013.03.001. Epub 2013 Mar 27.

Triptolide protects rat heart against pressure overload-induced cardiac fibrosis.

Author information

1
Department of Cardiology, the Second Clinic Medical College, Yangzhou University, Yangzhou, 225001, China; Department of Clinical Medicine, Yangzhou University Medical College, Yangzhou, 225001, China.

Abstract

BACKGROUND:

Emerging evidence underlines the role of inflammation activation in the process of cardiac fibrosis. Triptolide has potent anti-inflammatory and anti-proliferative properties, and extensively used in the treatment of chronic inflammatory disorders. In the current study, we test the hypothesis that triptolide treatment facilitates to attenuate chronic pressure overload-induced cardiac fibrosis in a model of rat.

METHODS:

Adult male Sprague-Dawley rats were subjected to a suprarenal abdominal aorta constriction (AC) or sham (as control) to induce sustained pressure overload. Eight weeks later, rats were randomly assigned to receive triptolide (9 μg/kg.d, i.p) or vehicle (0.1% dimethyl sulfoxide, 0.2 ml/d, i.p) treatment for an additional 8 weeks.

RESULTS:

AC caused significant pathological hypertrophy, cardiac fibrosis and reduced cardiac diastolic function. Triptolide treatment markedly inhibited AC-induced increases in myocardial collagen volume fraction, collagen type I/III deposition, left ventricular end-diastolic pressure, expressions of pro-fibrogenic factors (transforming growth factor-β and angiotensin II) and pro-inflammatory cytokines (IL-1β and IL-6), NF-κB activation and inflammatory cell infiltration in left ventricles compared with vehicle, without affecting cardiac hypertrophy. However, triptolide had no effects on systemic blood pressure and circulating angiotensin II level.

CONCLUSIONS:

Collectively, the findings suggested that triptolide treatment elicits favorable anti-fibrogenic effect in a blood pressure-independent manner, at least in part, through inhibiting myocardial pro-fibrogenic factor production and inflammatory activation in the pressure overloaded heart.

KEYWORDS:

Angiotensin II; Cardiac fibrosis; Inflammation; NF-κB; Triptolide

PMID:
23541609
DOI:
10.1016/j.ijcard.2013.03.001
[Indexed for MEDLINE]
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