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Triptolide protects rat heart against pressure overload‐induced cardiac fibrosis and inflammation activation
Author(s) -
Zhang Zhengang,
Ni Yue,
Zhang Kai,
Qin Jianhua,
Sun Hongguang,
Ding Yongling,
Zhao Pei,
Xing Dongqi,
Gong Kaizheng
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1031.1
Subject(s) - triptolide , pressure overload , inflammation , cardiac fibrosis , angiotensin ii , medicine , fibrosis , endocrinology , ventricular remodeling , heart failure , muscle hypertrophy , blood pressure , pharmacology , cardiac hypertrophy , chemistry , apoptosis , biochemistry
Emerging evidence underlines the role of inflammation activation in the process of cardiac remodeling. Triptolide has potent anti‐inflammatory and anti‐proliferative properties. In this study, we test the effect of triptolide on chronic pressure overload‐induced cardiac remodeling in rats. Male SD rats were subjected to a suprarenal abdominal aorta constriction (AC) or sham surgery. Eight weeks later, AC rats were daily treated with triptolide (9 μg/kg, i.p) or vehicle for additional 8 weeks. AC rats developed significant cardiac fibrosis, hypertrophy and inflammation activation compared with sham rats. Triptolide treatment markedly attenuated AC‐induced collagen type I/III deposition, myocardial IL‐1β, IL‐6 and transforming growth factor (TGF)‐β1 expression, as well as NF‐kB activity, but had no effects on cardiac hypertrophy, blood pressure and circulating angiotensin II level compared to vehicle treated AC rats. In isolated rat cardiac fibroblasts, triptolide inhibited angiotensin II‐induced IL‐1β, IL‐6 and TGF‐β1 secretion, as well as cellular proliferation and collagen production. Collectively, the findings suggested that inhibiting inflammation activation via directly antagonizing myocardial local angiotensin II may be a critical mechanism of anti‐fibrogenic action of triptolide in pressure overloaded heart. The work was supported by the National Natural Science Foundation of China (81070096), the Basic Research Project (Natural Science Foundation) of Jiangsu Province (BK2008220, BK2010324).