We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Eicosapentaenoic acid suppresses adverse effects of C-reactive protein overexpression on pressure overload-induced cardiac remodeling.
- Authors
Nagai, Toshiyuki; Anzai, Toshihisa; Mano, Yoshinori; Kaneko, Hidehiro; Anzai, Atsushi; Sugano, Yasuo; Maekawa, Yuichiro; Takahashi, Toshiyuki; Yoshikawa, Tsutomu; Fukuda, Keiichi
- Abstract
Serum C-reactive protein (CRP) elevation is associated with poor clinical outcome in patients with heart failure (HF). We previously reported that CRP exacerbates the development of pressure overload-induced cardiac remodeling through an enhanced inflammatory response and oxidative stress. In the present study, we examined the effect of eicosapentaenoic acid (EPA), a suppressor of inflammatory response and oxidative stress, on pressure overload-induced cardiac remodeling. Transverse aortic constriction (TAC) was performed on transgenic mice overexpressing CRP (CRPtg) and nontransgenic littermates (TAC/CON). CRPtg with TAC operation were randomly assigned to be fed a standard diet (TAC/CRPtg) or an EPA-enriched diet (7 % of total energy) (TAC/CRPtg/EPA). Myocardial mRNA level of transforming growth factor-β1, proinflammatory cytokines, and oxidative stress markers were increased in TAC/CRPtg in comparison with TAC/CON 1 and 4 weeks after the operation. These parameters were significantly suppressed in TAC/CRPtg/EPA compared with TAC/CRPtg. In addition, after 4 weeks of EPA treatment, as compared with TAC/CRPtg, TAC/CRPtg/EPA mice demonstrated reduced heart and lung weights, increased left ventricular fractional shortening, and decreased left ventricular end-diastolic pressure, together with decreased cardiac hypertrophy, fibrosis, and improved cardiac function. In conclusion, the anti-inflammatory and antioxidative properties of EPA may make it an effective therapeutic strategy for adverse cardiac remodeling associated with CRP overexpression.
- Subjects
EICOSAPENTAENOIC acid; C-reactive protein; GENE expression; VENTRICULAR remodeling; HEART failure; HEALTH outcome assessment; OXIDATIVE stress; INFLAMMATION
- Publication
Heart & Vessels, 2013, Vol 28, Issue 3, p404
- ISSN
0910-8327
- Publication type
Article
- DOI
10.1007/s00380-012-0270-5