Publications by authors named "Vanessa Touceda"
Sunflower oil is one of the most commonly used fat sources in Argentina, and deep-fat frying is the popular food preparation process. The liver response of feeding a diet containing fried sunflower oil (SFOx) on growing rats was studied. Thirty-nine male weanling Wistar rats were randomly assigned to one of three diets for 8 wks: control (C), sunflower oil (SFO), and a diet containing SFOx, both of the sunflower diets were mixed with a commercial rat chow at weight ratio of 13% (w/w).
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- Central obesity involves the growth of visceral fat, which increases metabolic risks, and recent drug studies, such as Liraglutide (LGT), aim to tackle this issue despite unclear mechanisms on how it impacts visceral fat.
- The study aimed to observe how LGT affects factors related to fat tissue remodeling and mitochondria in mice on a high-fat diet by categorizing them based on diet and drug administration.
- Results showed that LGT treatment led to smaller fat cells, increased blood vessel formation, improved fat tissue structure, and healthier mitochondria, indicating LGT's effectiveness in enhancing visceral fat behavior and functionality.
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- Doxorubicin (DOX) causes heart damage through direct injury to heart cells and inflammation, and this study investigates the impact of Galectin-3 (Gal-3), a protein linked to inflammation, on DOX-induced heart issues in mice.
- After administering DOX to both normal and Gal-3 knockout mice, results showed that the absence of Gal-3 led to lower heart injury markers, less oxidative stress, and improved heart function compared to normal mice.
- The study concludes that Gal-3's genetic deletion protects against heart damage caused by DOX, suggesting Gal-3 could be a potential target for treating heart toxicity in cancer patients receiving doxorubicin.
Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. This paper describes a protocol for studying the role of galectin 3 (Gal-3) in the temporal evolution of cardiac healing and remodeling in an experimental animal model of MI. The procedures described include an experimental model of MI with a permanent coronary ligature in male C57BL/6J (control) and Gal-3 knockout (KO) mice, an echocardiography procedure to study cardiac remodeling and systolic function in vivo, a histological evaluation of interstitial myocardial fibrosis with picrosirius red-stained and rhodamine-conjugated lectin-stained sections for studying myocyte hypertrophy by the cross-sectional area (MCSA), and the quantification of infarct size and cardiac remodeling (scar thinning, septum thickness, and expansion index) by planimetry in slices stained with Masson's trichrome and triphenyl tetrazolium chloride.
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- - The study investigates the role of galectin-3 (Gal-3) in age-related cardiac remodeling, positing that Gal-3 is crucial for protecting against myocardial hypertrophy and fibrosis as mice age.
- - Experiments with Gal-3 knockout (KO) mice showed a lower survival rate and more severe heart conditions, such as increased myocardial hypertrophy, fibrosis, and apoptosis, compared to control mice.
- - The results suggest that Gal-3 regulates key mechanisms involved in heart aging, and its absence leads to negative changes in heart structure and function, highlighting its importance in maintaining cardiac health in aged individuals.
Genetic Deletion of Galectin-3 Alters the Temporal Evolution of Macrophage Infiltration and Healing Affecting the Cardiac Remodeling and Function after Myocardial Infarction in Mice.
Am J Pathol
September 2020
We studied the role of galectin-3 (Gal-3) in the expression of alternative activation markers (M2) on macrophage, cytokines, and fibrosis through the temporal evolution of healing, ventricular remodeling, and function after myocardial infarction (MI). C57BL/6J and Gal-3 knockout mice (Lgals3) were subjected to permanent coronary ligation or sham. We studied i) mortality, ii) macrophage infiltration and expression of markers of alternative activation, iii) cytokine, iv) matrix metalloproteinase-2 activity, v) fibrosis, and vi) cardiac function and remodeling.
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