| Grant number: | 14/23229-6 |
| Support Opportunities: | Regular Research Grants |
| Start date: | March 01, 2015 |
| End date: | February 28, 2017 |
| Field of knowledge: | Health Sciences - Physical Education |
| Principal Investigator: | Sandra Lia do Amaral Cardoso |
| Grantee: | Sandra Lia do Amaral Cardoso |
| Host Institution: | Faculdade de Ciências (FC). Universidade Estadual Paulista (UNESP). Campus de Bauru. Bauru , SP, Brazil |
| City of the host institution: | Bauru |
| Associated researchers: | Carlos Ferreira dos Santos ; Valdecir Farias Ximenes |
Abstract
Dexamethasone (DEX) is widely used in clinics due to its potent effect as anti-allergic and anti-inflammatory drug, however its chronic use may cause several metabolic and haemodynamic alterations. It has been shown that DEX treatment provokes hypertension and muscle atrophy, however the mechanisms responsible for these effects are not totally understood. We recently have shown that renin-angiotensin system maybe not the main contributor for DEX- induced hypertension. On the other hand, reactive oxygen species (ROS) seems to be a common mechanism for hypertension and muscle atrophy but its involvement in hypertension and muscle atrophy induced by DEX needs to be investigated. Physical training has been considered a potent strategy in controlling hypertension and muscular atrophy, however, if its effects includes a better balance between ROS and anti-oxidant enzymes are not known. Therefore the main purpose of this study is to investigate if hypertension and muscle atrophy induced by DEX occurs due to an imbalance between production and removal of ROS and if the physical exercise attenuation of these side-effects involves an improvement on redox-balance. To answer these questions this study will associate functional (blood pressure and arterial stiffness) and structural (wall-to-lumen ratio and fibers transverse area section) techniques. These parameters will be associated with molecular evaluations, both gene expression and protein levels of mechanisms responsible for redox-status and muscle atrophy in sedentary and trained rats, treated or not with DEX. (AU)
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