Curcumin prevents the development of hypertension-induced left ventricular hypertrophy in ratas
Tomohide Takaya1, Tatsuya Morimoto1, Yoichi Sunagawa1, Hiromichi Wada1, Teruhisa Kawamura1, Akira Shimatsu1, Masatoshi Fujita2, Yoshiko Fujita3, Tatsuya Sawamura3, Koji Hasegawa1.
- Division of Translational Research, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan.
- Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
- Departemnt of Vascular Physiology, National Cardiovascular Center, Osaka, Japan.
The 17th Asian Pacific Congress of Cardiology (Kyoto, Japan), 2009/05/20 (Poster).
Abstract
Lectin-like oxidized low-density lipoprotein (oxLDL) receptor-1 (LOX-1) is a receptor for oxLDL and induced by proinflammatory cytokines and oxidative stress. Activated LOX-1 pathway in cardiomyocytes induces apoptosis in vitro and deteriorates ischemia-reperfusion injury in vivo. However, the role of LOX-1 in chronic heart failure remains unclear. We examined left ventricular (LV) expression of LOX-1 in a salt-sensitive Dahl (DS) rat model of hypertension. DS rats exhibited LV hypertrophy at 11 weeks, and decreased systolic function at 18 weeks. LV mRNA levels of LOX-1 indicated a 4.7-fold increase in DS rats compared with control salt-resistant Dahl (DR) rats at 11 weeks, and a 32-fold increase at 18 weeks. Immunohistochemistry revealed that LOX-1 expression in vessel walls and cardiomyocytes were greater in DS than DR rat hearts. The mRNA levels of LOX-1 were significantly correlated with blood pressure, LV/body weight ratio, LV wall thickness, and LV end-systolic dimension, and strongly correlated with the decrease of ejection fraction (r = -0.772) and the increases of BNP levels on plasma (r = 0.744) and mRNA (r = 0.814). Importantly, the mRNA levels of LOX-1 revealed the strongest correlation with a chemotactic factor MCP-1 (r = 0.943), and proinflammatory cytokines TGF-β1 (r = 0.936) and IL-1β (r = 0.760). These findings demonstrate that LV expression of LOX-1 is markedly increased in DS rat model of hypertension and possibly involved in chronic inflammation during the development of heart failure.