Exercise Training Prevents Dexamethasone-induced Rarefaction

Autor(es)

Herrera, Naiara A. ; Jesus, Isley ; Dionisio, Evandro J. ; Dionisio, Thiago J. ; Santos, Carlos F. ; Amaral, Sandra L.

• Tipo de documento: Artigo Científico
• Fonte: Journal of Cardiovascular Pharmacology; v. 70, n. 3, p. 194-201, SEP 2017.
• Citações Web of Science: 2

Resumo

Dexamethasone (DEX) causes rarefaction. In contrast, training (T) prevents rarefaction and stimulates angiogenesis. This study investigated the mechanisms responsible for the preventive role of T in DEX-induced rarefaction. Rats underwent T or were kept sedentary (8 weeks) and were treated with DEX or saline during the following 14 days. Tibialis anterior muscle was used for measurements of capillary density (CD), capillary-to-fiber ratio (C:F ratio), superoxide dismutase CuZn (SOD-1), superoxide dismutase MnSOD (SOD-2), catalase (CAT) mRNA as well as SOD-1, SOD-2, CAT, vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor-2 (VEGF-R2), cyclooxygenase-2 (COX-2), B-cell lymphoma 2 (Bcl-2), Bd-2-like protein 4 (Bax), p-Bax, and caspase-3 cleaved protein levels. DEX decreased CD (-38.1%), C: F ratio (-30.0%), VEGF (-19.0%), VEGFR-2 (-20.1%), COX-2 (-22.8%), Bcl-2 (-20.5%), Bcl-2/Bax ratio (-13.7%), p-Bax/Bax (-20.0%) and increased SOD-2 (+41.6%) and caspase-3 cleaved (+24.1%). Conversely, T prevented reductions in CD (+54.2%), C: F ratio (+32.9%), VEGF (+25.3%), VEGFR-2 (+22.2%), COX-2 (+31.5%), Bcl-2 (+35.5%), Bcl-2/Bax ratio (+19.9%), p-Bax/Bax (+32.1%), and caspase-3 cleaved increase (27.8%). T increased CAT mRNA (+21.5%) in the DEX-treated group. In conclusion, T prevented the DEX-induced rarefaction by increasing antioxidant enzymes resulting in a better balance between apoptotic and antiapoptotic protein levels. (AU)

• Processo FAPESP: 14/23229-6 - Efeitos do treinamento físico na hipertensão, enrijecimento arterial e atrofia muscular induzidos por dexametasona: papel do estresse oxidativo
• Beneficiário: Sandra Lia do Amaral Cardoso
• Modalidade de apoio: Auxílio à Pesquisa - Regular