Rosemary supplementation (Rosmarinus oficinallis L.) attenuates cardiac remodeling after myocardial infarction in rats.

BACKGROUND: Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. Dietary intervention on adverse cardiac remodeling after MI has significant clinical relevance. Rosemary leaves are a natural product with antioxidant/anti-inflammatory properties, but its effect on morphology and ventricular function after MI is unknown. METHODS AND RESULTS: To determine the effect of the dietary supplementation of rosemary leaves on cardiac remodeling after MI, male Wistar rats were divided into 6 groups after sham procedure or experimental induced MI: 1) Sham group fed standard chow (SR0, n = 23); 2) Sham group fed standard chow supplemented with 0.02% rosemary (R002) (SR002, n = 23); 3) Sham group fed standard chow supplemented with 0.2% rosemary (R02) (SR02, n = 22); 4) group submitted to MI and fed standard chow (IR0, n = 13); 5) group submitted to MI and fed standard chow supplemented with R002 (IR002, n = 8); and 6) group submitted to MI and fed standard chow supplemented with R02 (IR02, n = 9). After 3 months of the treatment, systolic pressure evaluation, echocardiography and euthanasia were performed. Left ventricular samples were evaluated for: fibrosis, cytokine levels, apoptosis, energy metabolism enzymes, and oxidative stress. Rosemary dietary supplementation attenuated cardiac remodeling by improving energy metabolism and decreasing oxidative stress. Rosemary supplementation of 0.02% improved diastolic function and reduced hypertrophy after MI. Regarding rosemary dose, 0.02% and 0.2% for rats are equivalent to 11 mg and 110 mg for humans, respectively. CONCLUSION: Our findings support further investigations of the rosemary use as adjuvant therapy in adverse cardiac remodeling.

Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity.

AIMS: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship. MAIN METHODS: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC). KEY FINDINGS: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation. SIGNIFICANCE: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphorylations in this animal model.