Omega-3 PUFA attenuate mice myocardial infarction injury by emerging a protective eicosanoid pattern.

Omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation is a recommended preventive approach against cardiovascular diseases, but its mechanism of protection against myocardial infarction (MI) injury is not fully understood. Eicosanoid metabolomics demonstrated an abnormal eicosanoid profile was in the plasma of mice receiving MI surgery. 19,20-EDP, 17,18-EEQ, 14,15-EET and 9,10-EpOME were decreased, and PGE2 was increased by the surgery. N-3 PUFA-rich diets feeding or transgene of Fat-1 shifted the eicosanoid profile to an n-3 PUFA dominant style and attenuated the myocardial infarction injury. Multiple logistic regression analysis suggested the degree of MI injury was related with an eicosanoid pattern, composed by eicosanoids derived from both n-3 and n-6 PUFA in the three enzymatic pathways. These results suggested the benefits of n-3 PUFA on MI was achieved synergistically.

Cardiomyocyte proliferation: remove brakes and push accelerators.

Adult mammalian hearts cannot repair by themselves after injury due to limited proliferation of cardiomyocytes; removal of cell cycle blocker and/or addition of drugs that boost proliferation of cardiomyocytes provide potential means to cardiac regeneration. Three publications that appeared recently in Nature and Cell Research now provide new hope to the treatment of heart injuries.

Multi-Strain Probiotics Inhibit Cardiac Myopathies and Autophagy to Prevent Heart Injury in High-Fat Diet-Fed Rats.

High-fat diets induce obesity, leading to cardiomyocyte fibrosis and autophagy imbalance. In addition, no previous studies have indicated that probiotics have potential health effects associated with cardiac fibrosis and autophagy in obese rats. This study investigates the effects of probiotics on high-fat (HF) diet-induced obesity and cardiac fibrosis and autophagy in rat hearts. Eight-week-old male Wistar rats were separated randomly into five equally sized experimental groups: Normal diet (control) and high-fat (HF) diet groups and groups fed a high-fat diet supplemented with low (HL), medium (HM) or high (HH) doses of multi-strain probiotic powders. These experiments were designed for an 8-week trial period. The myocardial architecture of the left ventricle was evaluated using Masson's trichrome staining and immunohistochemistry staining. Key probiotics-related pathway molecules were analyzed using western blotting. Abnormal myocardial architecture and enlarged interstitial spaces were observed in HF hearts. These interstitial spaces were significantly decreased in groups provided with multi-strain probiotics compared with HF hearts. Western blot analysis demonstrated that key components of the TGF/MMP2/MMP9 fibrosis pathways and ERK5/uPA/ANP cardiac hypertrophy pathways were significantly suppressed in probiotic groups compared to the HF group. Autophagy balance is very important in cardiomyocytes. In this study, we observed that the beclin-1/LC3B/Atg7 autophagy pathway in HF was increased after probiotic supplementation was significantly decreased. Together, these results suggest that oral administration of probiotics may attenuate cardiomyocyte fibrosis and cardiac hypertrophy and the autophagy-signaling pathway in obese rats.